Type I Interferon Regulates Cytokine-Delayed Neutrophil
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Correlation of Cytokine Level with the Severity of Severe Fever With
Liu et al. Virology Journal (2017) 14:6 DOI 10.1186/s12985-016-0677-1 RESEARCH Open Access Correlation of cytokine level with the severity of severe fever with thrombocytopenia syndrome Miao-Miao Liu1, Xiao-Ying Lei1, Hao Yu2, Jian-zhi Zhang3 and Xue-jie Yu1,4* Abstract Background: Severe fever with thrombocytopenia syndrome (SFTS) was an emerging hemorrhagic fever that was caused by a tick-borne bunyavirus, SFTSV. Although SFTSV nonstructural protein can inhibit type I interferon (IFN-I) production Ex Vivo and IFN-I played key role in resistance SFTSV infection in animal model, the role of IFN-I in patients is not investigated. Methods: We have assayed the concentration of IFN-α, a subtype of IFN-I as well as other cytokines in the sera of SFTS patients and the healthy population with CBA (Cytometric bead array) assay. Results: The results showed that IFN-α, tumor necrosis factor (TNF-α), granulocyte colony-stimulating factor (G-CSF), interferon-γ (IFN-γ), macrophage inflammatory protein (MIP-1α), interleukin-6 (IL-6), IL-10, interferon-inducible protein (IP-10), monocyte chemoattractant protein (MCP-1) were significantly higher in SFTS patients than in healthy persons (p < 0.05); the concentrations of IFN-α, IFN-γ, G-CSF, MIP-1α, IL-6, and IP-10 were significant higher in severe SFTS patients than in mild SFTS patients (p < 0.05). Conclusion: The concentration of IFN-α as well as other cytokines (IFN-γ, G-CSF, MIP-1α, IL-6, and IP-10) is correlated with the severity of SFTS, suggesting that type I interferon may not be significant in resistance SFTSV infection in humans and it may play an import role in cytokine storm. -
Primary Sjogren Syndrome: Focus on Innate Immune Cells and Inflammation
Review Primary Sjogren Syndrome: Focus on Innate Immune Cells and Inflammation Chiara Rizzo 1, Giulia Grasso 1, Giulia Maria Destro Castaniti 1, Francesco Ciccia 2 and Giuliana Guggino 1,* 1 Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties, Rheumatology Section, University of Palermo, Piazza delle Cliniche 2, 90110 Palermo, Italy; [email protected] (C.R.); [email protected] (G.G.); [email protected] (G.M.D.C.) 2 Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, Via L. De Crecchio 7, 80138 Naples, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-091-6552260 Received: 30 April 2020; Accepted: 29 May 2020; Published: 3 June 2020 Abstract: Primary Sjogren Syndrome (pSS) is a complex, multifactorial rheumatic disease that mainly targets salivary and lacrimal glands, inducing epithelitis. The cause behind the autoimmunity outbreak in pSS is still elusive; however, it seems related to an aberrant reaction to exogenous triggers such as viruses, combined with individual genetic pre-disposition. For a long time, autoantibodies were considered as the hallmarks of this disease; however, more recently the complex interplay between innate and adaptive immunity as well as the consequent inflammatory process have emerged as the main mechanisms of pSS pathogenesis. The present review will focus on innate cells and on the principal mechanisms of inflammation connected. In the first part, an overview of innate cells involved in pSS pathogenesis is provided, stressing in particular the role of Innate Lymphoid Cells (ILCs). Subsequently we have highlighted the main inflammatory pathways, including intra- and extra-cellular players. -
MST1 Is a Key Regulator of Beta Cell Apoptosis and Dysfunction in Diabetes
ARTICLES MST1 is a key regulator of beta cell apoptosis and dysfunction in diabetes Amin Ardestani1, Federico Paroni1,6, Zahra Azizi1,6, Supreet Kaur1,6, Vrushali Khobragade1, Ting Yuan1, Thomas Frogne2, Wufan Tao3, Jose Oberholzer4, Francois Pattou5, Julie Kerr Conte5 & Kathrin Maedler1 Apoptotic cell death is a hallmark of the loss of insulin-producing beta cells in all forms of diabetes mellitus. Current treatments fail to halt the decline in functional beta cell mass, and strategies to prevent beta cell apoptosis and dysfunction are urgently needed. Here, we identified mammalian sterile 20–like kinase-1 (MST1) as a critical regulator of apoptotic beta cell death and function. Under diabetogenic conditions, MST1 was strongly activated in beta cells in human and mouse islets and specifically induced the mitochondrial-dependent pathway of apoptosis through upregulation of the BCL-2 homology-3 (BH3)-only protein BIM. MST1 directly phosphorylated the beta cell transcription factor PDX1 at T11, resulting in the latter’s ubiquitination and degradation and thus in impaired insulin secretion. MST1 deficiency completely restored normoglycemia, beta cell function and survival in vitro and in vivo. We show MST1 as a proapoptotic kinase and key mediator of apoptotic signaling and beta cell dysfunction and suggest that it may serve as target for the development of new therapies for diabetes. Pancreatic beta cell death is the fundamental cause of type 1 diabetes of events, which makes the initiation of beta cell death complex and (T1D) and a contributing factor to the reduced beta cell mass in type 2 its blockade difficult to successfully achieve in vivo. -
Interactions Between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Auto-Immune Diseases
Type 1 interferons and the Th17 response in TB 1 http://hdl.handle.net/1765/106444 Interactions between type 1 interferons and the Th17 response in tuberculosis: Lessons learned from auto-immune diseases Bas C. Mourik1, Erik Lubberts2, Jurriaan E.M. de Steenwinkel1, Tom H.M. Ottenhoff3, Pieter J.M. Leenen4* 1Dept.Interactions of Medical Microbiology & between Infectious Diseases, Erasmus type MC, Rotterdam,1 interferons the Netherlands 2Dept.and of Rheumatology, the Th17 Erasmus MC, response Rotterdam, the Netherlands in tuberculosis: 3Dept.2 of Immunology, Erasmus MC, Rotterdam, the Netherlands Lessons learned from auto-immune 4Dept. of Infectious Diseases, LUMC, Leiden, the Netherlands Publisheddiseases in Frontiers in Immunology 2017 Apr 5;8:294. doi: 10.3389/fimmu.2017.00294. eCollection 2017 Bas C. Mourik1, Erik Lubberts2, Jurriaan E.M. de Steenwinkel1, Tom H.M. Ottenhoff3, Pieter J.M. Leenen4* 1Dept. of Medical Microbiology & Infectious Diseases, Erasmus MC, Rotterdam, the Netherlands 2Dept. of Rheumatology, Erasmus MC, Rotterdam, the Netherlands 3Dept. of Immunology, Erasmus MC, Rotterdam, the Netherlands 4Dept. of Infectious Diseases, LUMC, Leiden, the Netherlands Published in Frontiers in Immunology 2017 Apr 5;8:294. doi: 10.3389/fimmu.2017.00294. eCollection 2017 2 Erasmus Medical Center Rotterdam ABSTRACT The classical paradigm of TB immunity, with a central protective role for Th1 responses and IFN-γ-stimulated cellular responses, has been challenged by unsatisfactory results of vaccine strategies aimed at enhancing Th1 immunity. Moreover, preclinical TB models have shown that increasing IFN-γ responses in the lungs is more damaging to the host than to the pathogen. Type 1 interferon signaling and altered Th17 responses have also been associated with active TB, but their functional roles in TB pathogenesis remain to be established. -
Interferon Type I Responses in Primary and Secondary Infections
Immunology and Cell Biology (2008) 86, 239–245 & 2008 Australasian Society for Immunology Inc. All rights reserved 0818-9641/08 $30.00 www.nature.com/icb REVIEW Interferon type I responses in primary and secondary infections Mohammed Alsharifi, Arno Mu¨llbacher and Matthias Regner The mammalian host responds to a microbial infection with a rapid innate immune reaction that is dominated by type I interferon (IFN-I) release. Most cells of vertebrates can respond to microbial attack with IFN-I production, but the cell type responsible for most of the systemic IFN-I release is thought to be plasmacytoid dendritic cells (pDCs). Besides its anti- microbial and especially anti-viral properties IFN-I also exerts a regulatory role on many facets of the sequential adaptive immune response. One of these is being the recently described partial, systemic activation of the vast majority of B and T lymphocytes in mice, irrespective of antigen reactivity. The biological significance of this partial activation of lymphocytes is at present speculative. Secondary infections occurring within a short time span of a primary infection fail to elicit a similar lymphocyte activation response due to a refractory period in systemic IFN-I production. This period of exhaustion in IFN-I responses is associated with an increased susceptibility of the host to secondary infections. The latter correlates with well- established clinical observations of heightened susceptibility of patients to secondary microbial infections after viral episodes. Immunology and Cell Biology (2008) 86, 239–245; doi:10.1038/sj.icb.7100159; published online 8 January 2008 Keywords: type I interferon; immunoregulation; viral infections Control of viral infections by the vertebrate host involves both the fibroblast (b) and immune (g).2,3 The currently accepted classification innate and the adaptive immune response. -
Mice in Inflammation Psoriasiform Skin IL-22 Is Required for Imiquimod-Induced
IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle, Magali de Heusch, Muriel M. Lemaire, Emilie Hendrickx, Guy Warnier, Kyri This information is current as Dunussi-Joannopoulos, Lynette A. Fouser, Jean-Christophe of September 29, 2021. Renauld and Laure Dumoutier J Immunol published online 30 November 2011 http://www.jimmunol.org/content/early/2011/11/30/jimmun ol.1102224 Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 29, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2011 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published November 30, 2011, doi:10.4049/jimmunol.1102224 The Journal of Immunology IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice Astrid B. Van Belle,*,† Magali de Heusch,*,† Muriel M. Lemaire,*,† Emilie Hendrickx,*,† Guy Warnier,*,† Kyri Dunussi-Joannopoulos,‡ Lynette A. Fouser,‡ Jean-Christophe Renauld,*,†,1 and Laure Dumoutier*,†,1 Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes. -
Physical Exercise and Myokines: Relationships with Sarcopenia and Cardiovascular Complications
International Journal of Molecular Sciences Review Physical Exercise and Myokines: Relationships with Sarcopenia and Cardiovascular Complications Sandra Maria Barbalho 1,2,3,* , Uri Adrian Prync Flato 1,2 , Ricardo José Tofano 1,2, Ricardo de Alvares Goulart 1, Elen Landgraf Guiguer 1,2,3 , Cláudia Rucco P. Detregiachi 1 , Daniela Vieira Buchaim 1,4, Adriano Cressoni Araújo 1,2 , Rogério Leone Buchaim 1,5, Fábio Tadeu Rodrigues Reina 1, Piero Biteli 1, Daniela O. B. Rodrigues Reina 1 and Marcelo Dib Bechara 2 1 Postgraduate Program in Structural and Functional Interactions in Rehabilitation, University of Marilia (UNIMAR), Avenue Hygino Muzzy Filho, 1001, Marília 17525-902, São Paulo, Brazil; urifl[email protected] (U.A.P.F.); [email protected] (R.J.T.); [email protected] (R.d.A.G.); [email protected] (E.L.G.); [email protected] (C.R.P.D.); [email protected] (D.V.B.); [email protected] (A.C.A.); [email protected] (R.L.B.); [email protected] (F.T.R.R.); [email protected] (P.B.); [email protected] (D.O.B.R.R.) 2 School of Medicine, University of Marília (UNIMAR), Avenida Higino Muzzi Filho, 1001, Marília 17506-000, São Paulo, Brazil; [email protected] 3 Department of Biochemistry and Nutrition, Food Technology School, Marília 17525-902, São Paulo, Brazil 4 Medical School, University Center of Adamantina (UniFAI), Adamantina 17800-000, São Paulo, Brazil 5 Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo (FOB–USP), Alameda Doutor Octávio Pinheiro Brisolla, 9-75, Bauru 17012901, São Paulo, Brazil * Correspondence: [email protected]; Tel.: +55-14-99655-3190 Received: 6 May 2020; Accepted: 19 May 2020; Published: 20 May 2020 Abstract: Skeletal muscle is capable of secreting different factors in order to communicate with other tissues. -
Induced CNS Expression of CXCL1 Augments Neurologic Disease in a Murine Model of Multiple Sclerosis Via Enhanced Neutrophil Recruitment
Eur. J. Immunol. 2018. 48: 1199–1210 DOI: 10.1002/eji.201747442 Jonathan J. Grist et al. 1199 Basic Immunodeficiencies and autoimmunity Research Article Induced CNS expression of CXCL1 augments neurologic disease in a murine model of multiple sclerosis via enhanced neutrophil recruitment Jonathan J. Grist1, Brett S. Marro3, Dominic D. Skinner1, Amber R. Syage1, Colleen Worne1, Daniel J. Doty1, Robert S. Fujinami1,2 andThomasE.Lane1,2 1 Department of Pathology, Division of Microbiology and Immunology, University of Utah, School of Medicine, Salt Lake City, UT, USA 2 Immunology, Inflammation, and Infectious Disease Initiative, University of Utah, UT, USA 3 Department of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA Increasing evidence points to an important role for neutrophils in participating in the pathogenesis of the human demyelinating disease MS and the animal model EAE. There- fore, a better understanding of the signals controlling migration of neutrophils as well as evaluating the role of these cells in demyelination is important to define cellular com- ponents that contribute to disease in MS patients. In this study, we examined the func- tional role of the chemokine CXCL1 in contributing to neuroinflammation and demyeli- nation in EAE. Using transgenic mice in which expression of CXCL1 is under the control of a tetracycline-inducible promoter active within glial fibrillary acidic protein-positive cells, we have shown that sustained CXCL1 expression within the CNS increased the severity of clinical and histologic disease that was independent of an increase in the frequency of encephalitogenic Th1 and Th17 cells. Rather, disease was associated with enhanced recruitment of CD11b+Ly6G+ neutrophils into the spinal cord. -
Multiple Regulatory Regions on the 5' Side of the Mouse Ea Gene
Proc. Nad. Acad. Sci. USA Vol. 85, pp. 3075-3079, May 1988 Immunology Multiple regulatory regions on the 5' side of the mouse Ea gene (major histocompatibility genes/y-interferon/y-interferon response region) DIMITRIS THANOS*, GEORGE MAVROTHALASSITIS*, AND JOSEPH PAPAMATHEAKIS*t *Institute of Molecular Biology and Biotechnology, Research Center of Crete, P.O. Box 1527, and tDepartment of Biology, University of Crete, 711 10 Heraklion, Crete, Greece Communicated by Fotis C. Kafatos, December 10, 1987 ABSTRACT The function of the 5'-flanking region of the motifs in the 5'-flanking region of all major histocompatibil- mouse major histocompatibility complex gene E4 has been ity complex class II genes (15, 16). We provide evidence that studied by deletion analysis with the chloramphenicol acetyl- the CS are elements necessary for the inducibility by IFN-y. transferase gene as a transient expression marker in various cell lines. This analysis reveals the presence of several control regions on the 5' side of the gene. Sequences between base pair MATERIALS AND METHODS (bp) -873 and bp -353 have a negative function in human Plasmid Constructions. The following vectors were used and mouse fibroblasts but not in the mouse macrophage line for cloning Ea and E1n gene fragments. pL51CAT was derived WEHI-3. Additional positive and negative elements have been from pSV2CAT (17) by replacing the 350-base-pair (bp) Acc mapped between bp - 353 and bp - 38. A V-interferon I-Sph I fragment by a pUC19 polylinker. pLSVOCAT was response region has been also identified within that sequence. derived from pL51CAT by elimination of the 150-bp Sma I The 5' and 3' boundaries of the -interferon response region (polylinker)-HindIII fragment. -
The Chemokine System in Innate Immunity
Downloaded from http://cshperspectives.cshlp.org/ on September 28, 2021 - Published by Cold Spring Harbor Laboratory Press The Chemokine System in Innate Immunity Caroline L. Sokol and Andrew D. Luster Center for Immunology & Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114 Correspondence: [email protected] Chemokines are chemotactic cytokines that control the migration and positioning of immune cells in tissues and are critical for the function of the innate immune system. Chemokines control the release of innate immune cells from the bone marrow during homeostasis as well as in response to infection and inflammation. Theyalso recruit innate immune effectors out of the circulation and into the tissue where, in collaboration with other chemoattractants, they guide these cells to the very sites of tissue injury. Chemokine function is also critical for the positioning of innate immune sentinels in peripheral tissue and then, following innate immune activation, guiding these activated cells to the draining lymph node to initiate and imprint an adaptive immune response. In this review, we will highlight recent advances in understanding how chemokine function regulates the movement and positioning of innate immune cells at homeostasis and in response to acute inflammation, and then we will review how chemokine-mediated innate immune cell trafficking plays an essential role in linking the innate and adaptive immune responses. hemokines are chemotactic cytokines that with emphasis placed on its role in the innate Ccontrol cell migration and cell positioning immune system. throughout development, homeostasis, and in- flammation. The immune system, which is de- pendent on the coordinated migration of cells, CHEMOKINES AND CHEMOKINE RECEPTORS is particularly dependent on chemokines for its function. -
Critical Role of CXCL4 in the Lung Pathogenesis of Influenza (H1N1) Respiratory Infection
ARTICLES Critical role of CXCL4 in the lung pathogenesis of influenza (H1N1) respiratory infection L Guo1,3, K Feng1,3, YC Wang1,3, JJ Mei1,2, RT Ning1, HW Zheng1, JJ Wang1, GS Worthen2, X Wang1, J Song1,QHLi1 and LD Liu1 Annual epidemics and unexpected pandemics of influenza are threats to human health. Lung immune and inflammatory responses, such as those induced by respiratory infection influenza virus, determine the outcome of pulmonary pathogenesis. Platelet-derived chemokine (C-X-C motif) ligand 4 (CXCL4) has an immunoregulatory role in inflammatory diseases. Here we show that CXCL4 is associated with pulmonary influenza infection and has a critical role in protecting mice from fatal H1N1 virus respiratory infection. CXCL4 knockout resulted in diminished viral clearance from the lung and decreased lung inflammation during early infection but more severe lung pathology relative to wild-type mice during late infection. Additionally, CXCL4 deficiency decreased leukocyte accumulation in the infected lung with markedly decreased neutrophil infiltration into the lung during early infection and extensive leukocyte, especially lymphocyte accumulation at the late infection stage. Loss of CXCL4 did not affect the activation of adaptive immune T and B lymphocytes during the late stage of lung infection. Further study revealed that CXCL4 deficiency inhibited neutrophil recruitment to the infected mouse lung. Thus the above results identify CXCL4 as a vital immunoregulatory chemokine essential for protecting mice against influenza A virus infection, especially as it affects the development of lung injury and neutrophil mobilization to the inflamed lung. INTRODUCTION necrosis factor (TNF)-a, interleukin (IL)-6, and IL-1b, to exert Influenza A virus (IAV) infections cause respiratory diseases in further antiviral innate immune effects.2 Meanwhile, the innate large populations worldwide every year and result in seasonal immune cells act as antigen-presenting cells and release influenza epidemics and unexpected pandemic. -
Exploration of Prognostic Biomarkers and Therapeutic Targets in the Microenvironment of Bladder Cancer Based on CXC Chemokines
Exploration of Prognostic Biomarkers and Therapeutic Targets in The Microenvironment of Bladder Cancer Based on CXC Chemokines Xiaoqi Sun Department of Urology, Kaiping Central Hospital, Kaiping, 529300, China Qunxi Chen Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China Lihong Zhang Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China Jiewei Chen Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China Xinke Zhang ( [email protected] ) Sun Yat-sen University Cancer Center Research Keywords: Bladder cancer, Biomarkers, CXC Chemokines, Microenvironment Posted Date: February 24th, 2021 DOI: https://doi.org/10.21203/rs.3.rs-223127/v1 License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License Page 1/29 Abstract Background: Bladder cancer (BLCA) has a high rate of morbidity and mortality, and is considered as one of the most malignant tumors of the urinary system. Tumor cells interact with surrounding interstitial cells, playing a key role in carcinogenesis and progression, which is partly mediated by chemokines. CXC chemokines exert anti‐tumor biological roles in the tumor microenvironment and affect patient prognosis. Nevertheless, their expression and prognostic values patients with BLCA remain unclear. Methods: We used online tools, including Oncomine, UALCAN, GEPIA, GEO databases, cBioPortal, GeneMANIA, DAVID 6.8, Metascape, TRUST (version 2.0), LinkedOmics, TCGA, and TIMER2.0 to perform the relevant analysis. Results: The mRNA levels of C-X-C motif chemokine ligand (CXCL)1, CXCL5, CXCL6, CXCL7, CXCL9, CXCL10, CXCL11, CXCL13, CXCL16, and CXCL17 were increased signicantly increased, and those of CXCL2, CXCL3, and CXCL12 were decreased signicantly in BLCA tissues as assessed using the Oncomine, TCGA, and GEO databases.