2231st Conference Immunology Summit & Immunity and Immunotherapies 2018
10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Poster Presentations
Page 45 Daniel Horowitz et al., J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
The development of a novel 3D printed prototype device to simplify blood cell subset enrichment at clinical sites Daniel Horowitz, George Szabo, Rudolf Cedro Jr. and Ling-Yang Hao Janssen Pharmaceutical Companies of Johnson & Johnson, USA
eripheral blood collection is a relatively non-invasive way to obtain biomarkers during clinical trials. Protein and gene Pexpression changes can be used to assess drug/target engagement and disease state changes. To avoid functional changes in blood cells during storage, cells need to be stored in appropriate buffers. For gene expression analysis, whole blood can be collected in buffers that lyse the cells and protect RNA from degradation, but this obscures changes that may be found only in specific cell types. The separation of specific subsets requires instrumentation and trained personnel not readily available at many clinical sites, and shipping to a processing lab may affect the results. Therefore, a way to enrich for and stabilize blood cell subsets at the site of collection is needed. We have developed a portable 3D printed prototype device that can be operated with minimal training. Blood is collected into a tube containing commercially available polystyrene spheres (PluriSelect) coupled to an antibody specific for a blood cell surface antigen. After a 10 min incubation at room temperature, the tube is inserted into the device, followed by a single washing step. Between the inlet and outlet is a mesh with pores that are smaller than the polystyrene beads. All of the blood cells attached to the beads will remain on the mesh, while the unbound cells will pass through the filter. Using anti-CD3 antibodies, we were able to use FACS to verify that the device is capable of enriching more than 1,000,000 CD3+ cells from 2ml of whole blood with 90% purity. At a clinical site, these cells can be collected and processed at room temperature with minimal manipulation and stored in the appropriate buffer and transported. This prototype device may enable cell type-specific analysis for pharmacokinetic/pharmacodynamic assessments and biomarker discovery.
Biography Daniel Horowitz has a BA from Temple University and has worked at Janssen for the past 13 years in the Immunology therapeutic area. Projects include biomarker discovery and development of techniques to help progress compounds through early clinical development. Disease areas include Pulmonary disease and Inflammatory bowel disease.
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Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 46 Jamal Almitairi, J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Activation of the classical complement pathway and auto-immune diseases Jamal Almitairi University of Leicester, United Kingdom
he classical pathway of complement activation triggers lysis and opsonization of invading pathogens and stimulates Tinflammatory and adaptive immune responses resulting in auto-immune diseases and graft-rejection in organ transplantation. It is initiated via large multicomponent assembly, known as C1 (790kDa), that binds to immune complexes, protein modulators (e.g., C-reactive protein), and polyanionic structures on pathogens and apoptotic cells. It is composed of a large recognition subcomponent, C1q (460kDa), with a bouquet-like architecture consisting of six collagenous stems, each linked to a globular head, and four serine protease subcomponents, two C1r polypeptides (90kDa) and two C1s polypeptides (80kDa) that in the absence of C1q form a Ca2+-dependent heterotetramer. Binding to pathogens induces auto-activation in a stepwise fashion: C1r auto- activates and then activates C1s. C1s subsequently cleaves substrates C4 and C4b-bound C2 to form the C3 convertase (C4b2a), the next enzyme in the pathway. Here we describe the structure of the C1r–C1s interaction in the form of a complex between the CUB1-EGF-CUB2 fragments of each protease highlighting the conformational changes during activation. The fragments form Ca2+-dependent heterodimers both in solution and in the crystals. The interface is extensive and spans all three domains of each protease. Supporting the traditional arrangement in which C1r-C1s heterodimers are linked via interactions between the catalytic domains of C1r. In association with C1q, the C1r-C1r contacts would prevent auto-activation of C1r as the proteases fold up with the C1r-C1s dimers at the center. Disruption of the C1r contacts when C1 binds to an activating surface very likely triggers auto-activation of C1r and subsequent activation of C1s. Activation is likely facilitated through hyper flexibility at the C1s EGFCUB2 junction, enabling considerable movement of the catalytic domains.
Biography Jamal Almitairi is a 3rd year PhD student at the University of Leicester working in structural biology and complement related diseases. Part of his work was published in the following journal: PNAS
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Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 47 Luay AL-Kanan, J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Characterisation of collections CL-Kl and CL-L1 and their role in the innate immune response Luay AL-Kanan University of Leicester, United Kingdom
he immune system is a collection of proteins, cells and other biological components that protect an organism against Tpathogenic microbes. It prevents an attack through a series of processes collectively called the immune response. The complement system is an essential part of the innate immune response. Complement is activated by three pathways: the Classical (CP), the Lectin (LP) and the Alternative pathways (AP). The LP is activated by a range of different pathogen- recognition receptors including collecting kidney-1 (CL-K1 aka CL-11) and collecting liver-1 (CL-L1 aka CL-10), which bind to pathogen-associated molecular patterns (PAMPs), to activate three MBL-associated serine proteases (MASPs). CL-K1 and CL-L1 play an important role in host defense by recognizing a range of pathogens. These proteins can activate the LP individually or as a hetero-oligomeric complex. The sugar specificity of CL-K1 has been analyzed recently, it binds to high- mannose type structures and a range of different fucose-containing sugars including Lewis antigens and Blood group antigens. Binding of the former have been characterized structurally but binding to fucose-containing structures has not. In addition, the sugar specificities of CL-L1 is unknown. Here we present structures highlighting the ligand binding by CL-L1 and CL-K1. CL-K1 is known to bind to mannose and fucose-containing sugars, which are commonly found on bacterial surfaces.
Biography Luay AL-Kanan PhD student working with Professor Wallis group in molecular biology and complement related disease.
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Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 48 Xiao-Lin Tian et al., J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Targeting both de novo biosynthesis and recycling of undecaprenyl phosphate as a new antimicrobial strategy against gram-positive bacteria Xiao-Lin Tian, Hasan Salim, Heather Rutherford and Yung-Hua Li Dalhousie University, Canada
ntimicrobial agents that target bacterial cell wall biosynthesis are among the most successful armamentaria against bacterial infections. It is well known that undecaprenyl phosphate (C -P or Up) is an essential lipid carrier required for cell wall A 55 biosynthesis. Up is synthesized both via the de novo biosynthesis from dephosphorylation of undecaprenyl pyrophosphate (Upp) in the cytoplasm and via the recycling of released Upp after glycan is transferred to other molecules outside the cytoplasm. Both reactions are catalyzed by undecaprenyl pyrophosphate phosphatase (UppP). In addition to this pathway, Streptococcus
mutans is found to have an alternative pathway to generate Up from phosphorylation of undecaprenol (C55-OH) catalyzed by an ortholog of diacylglycerol kinase (DagK). In this study, we aimed to determine whether simultaneous inactivation of uppP and dagK or blocking both the UppP- and DagK-catalyzed pathways affected the growth of S. mutans in response to cell wall-acting antibiotics. Two single-gene deletion mutants, ΔuppP and ΔdagK, and a double deletion mutant ΔdagK/uppP, were constructed for antibiotic susceptibility tests. The results revealed that deletion of uppP resulted in a mutant (ΔuppP) that was highly sensitive to bacitracin (MIC=0.25μg/mL), while deletion of dagK (ΔdagK) had much less effect (MIC≈20μg/mL) than the parent (MIC=40μg/mL). However, double deletion of both dagK and uppP nearly abolished the resistance of S. mutans to bacitracin, especially under pH 6.0. A combination of UppP inhibitor bacitracin (20μg/mL) with DgK inhibitor R59949 (25μM) almost completely inhibited the growth of S. mutans. It is concluded that antibacterial strategies that target both UppP- and DagK-catalyzed pathways could be an effective approach against Gram-positive bacteria such as S. mutans.
Biography Xiao-Lin Tian received her MD degree in the Shanghai First Medical University. Since 1993, she worked as a researcher for Novopharm Biotech Inc for six years. She then worked in the Mount Sinai Hospital Lunenfeld Research Institute, Toronto, for another six years. Since 2006, Xiao-Lin has been working as a researcher at Dalhousie University, with the expertise of bacterial pathogenesis.
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Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 49 Yung-Hua Li, J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Inactivation of the BceABRS four-component system attenuates the ability of Streptococcus mutans to survive in human blood and reduces its cariogenic potential in a rat caries model Yung-Hua Li Dalhousie University, Canada
treptococcus mutans is a primary etiological agent of dental caries worldwide. This bacterium may promote systemic Sinfections, such as infective endocarditis, after gaining access to bloodstream or bacteremia. We previously characterized a four-component system, BceABRS, which is essential for cell envelope stress response and required for biofilm formation and fitness of S. mutans. In this study, we provide evidence that the BceABRS system of S. mutans is also required for its survival in human blood and cariogenic potential in a rat caries model. An ex vivo blood survival assay revealed that a deletion of bceA, bceB, bceR or bceS resulted in a mutant that showed a reduced survival rate in blood compared with their parent strain, S. mutans UA159. Introducing a wild copy of each of these genes into the mutants in trans increased the survival rates of these strains in blood. Luciferase reporter assay showed that human serum-induced transcription of the bceABRS operon at a level similar to that by a physiological concentration of innate defense peptides, such as α-defensin-1 or β-defensin-3. Animal studies showed that all the BceABRS-deficient mutants had significantly reduced abilities for oral colonization and potential for initiation of dental caries based on mean caries scores from the animals: 30.5±7.2 for ΔbceA, 28.8±6.8 for ΔbceB, 30.2±7.4 for ΔbceR and 30.8±6.5 for ΔbceS compared with their parent UA159 (56.6±7.8) (P≤0.01-0.005). In conclusion, the BceABRS system in S. mutans is required for its survival in human blood and cariogenic potential in a rat caries model. Supported by CIHR grant MOP-115007 and by NSERC grant RGPIN 311682-07.
Biography Yung-Hua Li received his doctorate in molecular microbiology in the University of Manitoba. Following his postdoctoral fellowships in the University of Rochester, NY. She worked as a scientist in the University of Toronto, with his research focus on molecular dissection of microbial biofilms and pathogenesis. In 2004, she joined the Faculties of Dentistry and Medicine at Dalhousie University, where he has been directing a research team on microbiological and molecular analyses of bacterial pathogenesis, biofilms, and host-bacterial interactions.
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Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 50 Jacobus Hendricks, J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
The formation of mutated IgM memory B cells in rat splenic marginal zones is an antigen dependent process Jacobus Hendricks University of KwaZulu-Natal, South Africa
revious studies in rodents have indicated that only a minor fraction of the IGHV-Cµ transcripts carries somatic mutations, Pand is considered memory B cells. This is in marked contrast to humans where nearly all MZ-B cells are mutated. Here we show that the proportion of mutated IgM+ MZ-B cells varies significantly between the various IGHV genes analyzed, ranging from 27% mutated IGHV5 transcripts to 65% mutated IGHV4 transcripts. Excitingly we observed mutated sequences from clonally related B cells with a MZ-B cell and FO-B cell phenotype indicating that mutated IgM+ MZ-B and FO-B cells have a common origin. To report on the origin of mutated IgM MZ-B cells we have analysed whether rearranged IGHV-Cµ transcripts using IGHV4 and IGHV5 genes from neonatal MZ-B cells and follicular B (FO-B) cells carry mutations. We were not able to detect mutations in any of the IGHV4 and IGHV5 genes expressed by MZ-B cells or FO-B cells from neonatal rat spleen. Since GC’s are absent from neonatal rat spleen, these data argue against the notion that MZ-B cells mutate their IGHV genes as part of their developmental program, but are consistent with the notion that mutated rat MZ-B cells require GCs for their generation. Together we conclude that the splenic MZ of rats harbors a significant number of memory type IgM+ MZ-B cells with mutated immunoglobulin genes and that these memory MZ-B cells are probably generated as a result of an antigen driven immune response in germinal centers.
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Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 51 2231st Conference Immunology Summit & Immunity and Immunotherapies 2018
10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Accepted Abstracts
Page 53 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Human papillomavirus infection in genital women in four regions of Senegal El Hadji Seydou Mbaye1,2,3, Tarik Gheit1, Ahmadou Dem3, Sandrine McKay-Chopin1, Ndeye Coumba Toure-Kane2, Souleymane Mboup2, Massimo Tommasino1, Bakary S Sylla1 and Cheikh Saad Bouh Boye2 1International Agency for Research on Cancer, France 2Laboratory of Bacteriology and Virology, Aristide Le Dantec Hospital, Senegal 3Cancer Institute, Aristide Le Dantec Hospital, Senegal
Introduction: Cervical cancer is the most frequent cancer among women in Senegal. However, there are few data concerning the HPV types inducing neoplasia and cervical cancers and their prevalence, in the general population of Senegal. Aims: The aim of this study is to determine the prevalence of HPV infection in Senegalese women aged from 18 years and older. Materials and Methods: A study was performed on 498 cervix samples collected from healthy women aged 18 and older in Dakar. 438 other samples were collected from three other regions, Thiès, Saint Louis and Louga. The samples were screened for 21 HPV genotypes using an HPV type-specific E7 PCR bead-based multiplex genotyping assay (TS-MPG) which is a laboratory-developed method for the detection of HPV. Results: The prevalence for pHR/HR-HPV in the region of Dakar was 20.68%. HPV 52 (3.21%) was the most prevalent HPV type, followed by HPV 16 (3.01%) and HPV 31 (3.01%). In the regions of Thiès, Louga and Saint Louis, the prevalence for pHR/HR-HPV was 29.19%, 23.15%, and 20%, respectively. Conclusion: The study revealed the specificity of the HR-HPV prevalence in Dakar and other regions of Senegal. The patterns differ from the one observed in the other regions of the world and raise the issue of the development of vaccination program in the country. Such a program should take into account the real HPV prevalence for an effective protection of HPV-associated diseases.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 54 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Binding of cholera toxin B subunit to intestinal epithelial cells Elena V Navolotskaya Branch of Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Federation
e have prepared 125I-labeled cholera toxin B subunit (125I-labeled CT-B, a specific activity of 98 Ci/mmol) and found that it Wbinds to rat intestinal epithelial cell membranes, rat IEC-6 and human Caco-2 intestinal epithelial cells with high affinity. The binding of labeled protein was completely inhibited by unlabeled thymosin-α1 (TM-α1), interferon-α2 (IFN-α2), and the synthetic peptide LKEKK that corresponds to residues 16-20 in TM-α1 and 131-135 in IFN-α2, but was not inhibited by the synthetic peptide KKEKL with the inverted amino acid sequence. Thus, TM-α1, IFN-α2, and the peptide LKEKK bind with high affinity and specificity to the cholera toxin receptor on rat intestinal epithelial cell membranes, IEC-6, and Caco-2 cells. It was found that CT-B and the peptide: LKEKK at concentrations of 10-1000nM increased in a dose-dependent manner the nitric oxide (NO) production and the soluble guanylate cyclase (sGC) activity in IEC-6 and Caco-2 cells. Taking into account that NO acts as a primary activator of sGC, it can be assumed that the effect of CT-B and the peptide: LKEKK on the target cell is realized in the following way: increase in the iNOS expression → increase in the NO production → increase in the sGC activity → increase in intracellular levels of cGMP
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 55 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
The immunostimulatory effects of sulfated polysaccharide extracted from the phaeophycean macroalgae MA 04 and MA 10 in Nile Tilapia, Oreochromis niloticus S Kalaivani Priyadarshini, A Preethi Jenifer and C Kanmai Lady Doak College, India
he sulfated polysaccharide fraction was extracted from 11 macroalgal candidates collected from Vadakadu, Rameswaram District, TTamil Nadu. The total sulfated polysaccharide fractionated from eleven macroalgal candidates was screened based on the yield and biochemical characterization of sulfate content, polysaccharide content and HPLC analysis, in order to examine the sulfated polysaccharide-rich candidate. Based on the result MA 04-SPF and MA 10- SPF was selected as a macroalgal candidate for measuring its immunomodulatory effect in Nile Tilapia, Oreochromis niloticus. The fish (n=10, each) were intraperitoneally administered with 2, 20 and 200mg mL-1 doses of Sulfated polysaccharide fraction (SPF) of either MA 04-SPF or MA 10-SPF and a control set was injected with saline and the nonspecific (Humoral and Cellular) immune parameters were measured. In general, all the doses of both MA 04-SPF and MA 10-SPF administered groups showed significantly (P≤0.05) enhanced the humoral non-specific immune response of serum lysozyme and myeloperoxidase activity. Regarding, cellular ROS production the lowest dose MA 04-SPF 2mg mL-1 administered group alone showed significantly enhanced response, whereas MA 10-SPF at the dose of 200 mg mL-1 showed suppression in ROS production than the control. It was surprisingly evident that both MA 04-SPF and MA 10-SPF does not show any modulation of cellular reactive nitrogen species production. Thus it is evident that the total sulfated polysaccharide fraction of MA 04 and MA 10 could serve as an efficacious immunostimulant to treat finfish diseases thereby boost up the aquaculture production.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 56 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Mycobacterium tuberculosis host cell interaction: Role of latency associated protein Acr-1 in differential modulation of macrophages Nida Mubin and Owais Mohammad Aligarh Muslim University, India
ycobacterium tuberculosis (M.tb) contrives intracellular abode as a strategy to combat antibody onslaught. Additionally, to Mthrive against hostile ambiance inside host macrophages, the pathogen inhibits phagolysosomal fusion. Finally, to further defy host cell offensives, M.tb opts for dormant phase, where it turns off or slows down most of its metabolic process as an added stratagem. While M.tb restrains most of its metabolic activities, surprisingly latency-associated alpha-crystallin protein (Acr-1) is expressed most prominently during dormancy. Interestingly, several previous studies described the potential of Acr-1 to induce a robust immuno-prophylactic response in the immunized host. It is intriguing to comprehend the apparent discrepancy that how the microbe M.tb overexpresses a protein that has the potential to prime host immune system against the pathogen itself. Keeping this apparent ambiguity into consideration, it is imperative to unravel the intricacies involved in the exploitation of Acr-1 by M.tb during its interaction with host immune cells. The present study suggests that Acr-1 exhibits a diverse role in the maturation of macrophages (MΦs) and related immunological responses. The early encounter (pre-exposure) of bone marrow-derived immune cells (during their differentiation to MΦs) with Acr-1 (AcrMΦpre), results in hampering of their function. The pre-exposure of naïve MΦ with Acr-1 modulates expression of TIM-3 and IL-10 as well. In contrast, exposure of fully differentiated MΦ to Acr-1 results in their activation. Furthermore, Acr-1 mediated activation of MΦ results in the induction of Th1 and Th17 phenotype by activated T lymphocyte.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 57 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Retrovirus-derived virus-like particles as tolerogenic vaccines for allergy treatment Pierre-Axel Vinot1,2, James Vigneron1, Béatrice Levacher, Thomas Vazquez, Fabien Pitoiset1,2, David Klatzmann1,2 and Bertrand Bellier1,2 1Sorbonne Université, France 2Centre d’Investigation Clinique BioThérapies, France
he rise of immune disorders in the last decades paved the way for the development of new therapeutic approaches such as Ttolerogenic vaccination. The rationale is to administer allergens in a specific formulation thus reinforcing allergen-specific Th1 and/or regulatory T cell responses. Among the different vector systems used to formulate allergens, we selected and designed a retrovirus-derived virus-like particles (VLP) to carry allergens into the core and display an inhibitory molecule on the surface using chimeric binding. Recombinant tolerogenic VLPs (tVLPs) with ovalbumin (OVA) as model antigen were produced and we investigated their regulatory activity on both human and murine dendritic cells (DCs). We showed that tVLPs downregulate the surface expression of costimulatory molecules (i.e. CD80, CD86) on DCs and induce a pro-tolerogenic cytokine secretion profile. The therapeutic efficacy against allergy was assessed in a murine model of OVA-induced food allergy. BALB/c mice sensitized to OVA were vaccinated with tVLPs and then challenged by OVA p.o administrations. tVLP vaccination significantly reduced the clinical signs of allergy and protected against anaphylactic reactions. Notably, we demonstrated that the induced protection is maintained over a 5 months period in vaccinated mice and was dependent on regulatory T cells. Altogether, our results support the proof of concept for the efficacy of a VLP-based tolerogenic vaccine against food allergy and the characterization of related mechanisms are under investigation.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 58 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Electron microscopic studies of brain tissue in fetuses from schizophrenic mothers Segundo Mesa Castillo Psychiatric Hospital of Havana, Cuba
he neurodevelopmental theory in the etiology of schizophrenia is considered one of the most consistent at present. Evidence Tfrom epidemiological and neuropathological studies indicates that the pathogenic process that culminates in the development of schizophrenia are initiated early in life and has been associated with a variety of prenatal environmental insults to the developing brain, including infection. Although the infectious agents have been proposed as one of the risk factors for schizophrenia the data on the association of a specific infectious agent with prenatal brain evidence is absent. Understanding of the structural abnormalities would allow a better identification of neurodevelopmental processes that contribute to risk for schizophrenia. We have hypothesized that at ultrahigh-risk fetuses would have alterations at the cellular level that would let us differentiate them from the comparison subjects. A reappraisal of our ultrastructural studies carried out in samples of the left temporal lobe of fetuses at ultra-high risk of developing schizophrenia is presented. The findings obtained are compatible with an active infection of the central nervous system by herpes simplex hominis type I [HSV1] virus. The present results are the first direct evidence that demonstrates the presence of this virus in the central nervous system of fetuses from schizophrenic mothers in the critical period of fetal development. The importance of this finding can have practical applications in the prevention of the illness keeping in mind its direct relation to the etiology and physiopathology of schizophrenia.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 59 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Direct evidence of viral infection and mitochondrial alterations in the brain of fetuses at high risk for schizophrenia Segundo Mesa Castillo Psychiatric Hospital of Havana, Cuba
Introduction: There is an increasing evidence that favors the prenatal beginning of schizophrenia. These shreds of evidence point toward intra-uterine environmental factors that act specifically during the second pregnancy trimester producing a direct damage to the brain of the fetus. The currently available technology doesn't allow observing what is happening at the cellular level since the human brain is not exposed to a direct analysis in that stage of the life in subjects at high risk of developing schizophrenia. Methods: In 1977, we began a direct electron microscopic research of the brain of fetuses at high risk from schizophrenic mothers in order to find differences at the cellular level in relation to controls. Results: In these studies, we have observed within the nuclei of neurons the presence of complete and incomplete viral particles that reacted in positive form with antibodies to herpes simplex hominis type I [HSV1] virus, and mitochondria alterations. Conclusion: The importance of these findings can have practical applications in the prevention of the illness keeping in mind its direct relation to the etiology and physiopathology of schizophrenia. A study of the gametes or the amniotic fluid cells in women at risk of having a schizophrenic offspring is considered. Of being observed the same alterations that those observed previously in the cells of the brain of the studied fetuses, it would intend to these women in risk of having a schizophrenia descendant, previous information of the results, the voluntary medical interruption of the pregnancy or an early anti HSV1 viral treatment as preventive measure of the later development of the illness
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 60 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Mutation characterization and heterodimer analysis of patients with leukocyte adhesion deficiency: Including one novel mutation Shahram Teimourian Iran University of Medical Sciences, Iran
Background and Aim: Leukocyte adhesion deficiency type 1 (LAD-I) is a rare, autosomal recessive disorder of neutrophil migration, characterized by severe, recurrent bacterial infections, inadequate pus formation and impaired wound healing. The ITGB2 gene encodes the β2 integrin subunit (CD18) of the leukocyte adhesion cell molecules and mutations in this gene cause LAD-I. The aim of the current study was to investigate the mutations in patients diagnosed with LAD-I and functional studies of the impact of two previously reported and a novel mutation on the expression of the CD18/CD11a heterodimer. Materials and Methods: Blood samples were taken from three patients who had signed the consent form. Genomic DNA was extracted and ITGB2 exons and flanking intronic regions were amplified by polymerase chain reaction. Mutation screening was performed after Sanger sequencing of PCR products. For functional studies, COS-7 cells were co-transfected with an expression vector containing cDNA encoding mutant CD18 proteins and normal CD11a. Flow cytometry analysis of CD18/CD11a expression was assessed by the dimer-specific IB4 monoclonal antibody. Results: Two previously reported mutations and one novel mutation,p. Cys562Tyr were found. All mutations reduced CD18/CD11 heterodimer expression. Conclusion: Our strategy recognized the p.Cys562Tyr mutation as a pathogenic alteration that does not support CD18 heterodimer formation. Therefore, it can be put into a panel of the carrier and prenatal diagnosis programs.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 61 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Down-regulation of inflammatory mediators’ gene expression in the liver, kidney, and pancreas of diabetic albino rats administered Asheitu Adams bitters Sunday Adeola Emaleku Adekunle Ajasin University, Nigeria
he inflammatory response is essentially an immune response to infections, injuries, drugs, toxic compounds etc., in order to Tmaintain tissue homeostasis under stressful conditions. However, if not regulated, it could result in increased concentrations of inflammatory mediators, which might lead to the occurrence of several chronic diseases, namely arthritis, diabetes, coronary diseases, neurological diseases, and cancer, among others via dysregulation of various signaling pathways. Asheitu Adams bitter (AAB) is a polyherbal medicine used as alternative therapy in the treatment of many ailments/diseases in Nigeria. This study was therefore conducted to comparatively investigate the effect of Asheitu Adams bitter on gene expressions of some inflammatory mediators in different tissues of diabetic albino rats. The animals were diabetes-induced using streptozotocin, and grouped into four groups of fives in addition to the non-diabetic control group consisting of five animals also. Groups four and five were orally administered AAB at 15mg/kg and 30mg/kg respectively, while group three were orally administered metformin (15mg/kg), and group one and two served as the non-diabetic and diabetic control respectively. The experiment lasted for twenty-five days before the animals were sacrificed and different tissues excised. Results showed that AAB down-regulated interleukins– IL-6, IL-1α, IL-1β, and monocyte chemoattractant protein-1 (MCP-1) genes in the kidney, liver, and pancreas but up-regulated IL-6, IL-1α, and IL-1β in intestinal crypt. Conclusively, AAB showed potentials for preventing chronic inflammation by down-regulating inflammatory mediators but could stimulate acute inflammation to maintain body homeostasis, which seems to be the route of administration dependent.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 62 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Potential immunological biomarkers for the detection of Mycobacterium tuberculosis infection in an endemic setting, Ethiopia Takele Teklu, Kwon Keehwan, Biniam Wondale, Milkessa HaileMariam, Mengistu Legesse, Girmay Medhin, Aboma Zewude, Rembert Pieper and Gobena Ameni University of Gondar, Ethiopia
ccurate diagnosis and early treatment of tuberculosis (TB) and latent TB infection (LTBI) are vital to prevent and control TB. The Alack of specific biomarkers hinders these efforts. This study’s purpose was to screen immunological markers that discriminate against M. tuberculosis (Mtb) infection outcomes in an endemic setting of Ethiopia. Whole blood from 90 participants was stimulated using the ESAT-6/CFP-10 antigen cocktail. The interferon-γ (IFN-γ)-based QuantiFERON diagnostic test was used to distinguish between LTBI and uninfected control cases. Forty cytokines/chemokines were detected from antigen-stimulated plasma supernatants (SPS) and unstimulated plasma samples (UPSs) using human cytokine/chemokine antibody microarrays. Statistical tests allowed us to identify potential biomarkers that distinguish the TB, LTBI, and healthy control groups. As expected, the levels of IFN-γ in SPSs returned a high receiver operating characteristic curve (AUC) value comparing healthy controls and LTBI cases (Z=0.911; P<0.001). The SPS data also indicated that IL-17 abundance discriminates LTBI from healthy controls (Z=0.763; P=0.001). RANTES and MIP- 1β were significantly elevated in SPSs of TB-infected compared to healthy controls (P<0.05), while IL-12p40 and sTNF-RII were significantly increased in active TB cases compared to the combined LTBI and control groups (P<0.05). Interestingly, quantitative changes for RANTES were observed using both SPSs and UPSs with P-values of 0.013 and 0.012, respectively, in active TB versus LTBI cases and 0.001 and 0.002, respectively, in active TB versus healthy controls. These results encourage biomarker verification studies for IL-17 and RANTES. Combinations of these cytokines may compliment IFN-γ measurements to diagnose LTBI and distinguish active TB from LTBI cases.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 63 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
Profile of cytotoxic Tcd8 cells in different forms of malaria in children Tariam Djibangar Agnes University Hospital Cocody, West Africa
he interested of my work talk about in Ivory Coast; malaria is hyperendemic and is transmitted throughout the year with an Tincreased rate during the rainy seasons. Its morbidity is 42.28% for a mortality of 15.29% in children under 5 years. In the issue of protection against severe forms of malaria in endemic areas, premunition or semi-protection has been mentioned as a protection factor acquired in adults after multiple infestations for several years. Multiclonal infections have been suggested to provide protection against malaria by preventing superinfection or by promoting tolerance to infection. However, the precise immunological mechanisms underlying this protection association are unknown. Despite that relative protection, 2 to 3% of adults living in endemic areas immunologically competent are victims of severe malaria (unpublished data Ivory Coast). That allows raising the question of susceptibility and resistance toward severe malaria. According to Adam E and al in animals, the susceptibility in the young rat to Plasmodium berghei is related to a low cytotoxic lymphocyte rate. According to Dassé et al., susceptibility in the young rat is related to the dendritic cell OX62, CD4- responsible for the humoral profile that appears to be ineffective in protecting the young rat against Plasmodium berghei while the dendritic cell OX62, CD4+ is more linked to resistance in adult animals. Those data should be confirmed in humans.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 64 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
The purpose of temperature of fever K M Yacob Marma Heatth Centre, India
hen the disease becomes threat to life or organs blood circulation decreases, temperature of fever will emerges to increase Wprevailing blood circulation. And it acts as a protective covering of the body to sustain life. When blood flow decrease to brain, the patient becomes fainted-delirious .If we try to decreases temperature of fever, the blood circulation will further reduced. Blood circulation never increases without temperature increase. Delirious can never be cured without increase in blood circulation. The temperature of fever is not a surplus temperature or it is not to be eliminated from the body. During fever, our body temperature increases like a brooding hen`s increased body temperature. The actual treatment to fever is to increase blood circulation. Two ways to increase blood circulation: 1. Never allow body temperature to lose 2. Apply heat from outside to the body. When the temperature produced by body due to fever and heat which we applied on the body combines together, the blood circulation increases. Then body will stop to produce heat to increase blood circulation. And body will get extra heat from outside without any usage of energy. How can we prove that the temperature of fever is to increase blood circulation If we ask any type of question related to fever by assuming that the temperature of fever is to increase blood circulation we will get a clear answer. If avoid or evade from this definition we will never get proper answer to even a single question. If we do any type of treatment by assuming that the temperature of fever is to increase blood circulation , the body will accept, at the same time body will resist whatever treatment to decrease blood circulation. No further evidence is required to prove the temperature of fever is to increase blood circulation.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
Page 65 J Clin Cell Immunol 2018, Volume: 9 DOI: 10.4172/2155-9899-C4-058 10th World Congress and Expo on Immunology, Immunity, Inflammation & Immunotherapies October 19-20, 2018 | New York, USA
During fever, why our body acts against facts of physics K M Yacob Marma Health Centre, India
ccording to the facts of physics, if temperature increases, thermal expansion of an object is positive it will expand and with the Adecrease in temperature, it will shrink. Pressure will increase due to an increase in temperature. On the contrary, during fever we can see blood vessels and skin are shrunk, pressure decreases, body shivers, sleep increases, motion decreases, inflammation increases, body pain increases, blood circulation decreases, dislike cold substances etc. In fever, the firing rate of Warm sensitive neurons decreases, and the firing rate of cold-sensitive neuron increases. At the same time if we apply hotness from outside by thermal bag or if we drink hot water, our body acts according to the Facts of Physics- increase of temperature pressure will also increase, expands blood vessels and skin, body sweats, motion will increase, inflammation will decrease, body pain will decrease, blood circulation will increase, like cold substances etc. During fever, why our body acts against Facts of Physics? When disease increases, pressure and temperature will decrease. Blood circulation will decrease due to a decrease of pressure. If the essential temperature of the body is going out, essential temperature and pressure will further decrease. This will further endanger the life or action of the organ. When disease increases, it is the sensible and discreet action of the brain that tends to act against facts of physics to sustain life or protect organ. There is no way other than this for a sensible and discreet brain to protect the life or organ. We will get a clear answer if we find out the purpose of fever, sensible and discreet action of the brain. No medical books clarify this. During fever, if the temperature of fever is not a surplus temperature or if it is not supposed to be eliminated from the body, the shrinking of skin and blood vessels, shivering of body, dislike towards cold substances etc., are a protective covering of the body to increase blood circulation to important organs of the body it is against the facts of physics.
Journal of Clinical & Cellular Immunology | ISSN: 2155-9899 | Volume: 9
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