DOCSLIB.ORG

Bone Loss -Induced Periodontal Tannerella Forsythia TLR2

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Bone Loss -Induced Periodontal Tannerella Forsythia TLR2 TLR2 Signaling and Th2 Responses Drive Tannerella forsythia-Induced Periodontal Bone Loss This information is current as Srinivas R. Myneni, Rajendra P. Settem, Terry D. Connell, of October 4, 2021. Achsah D. Keegan, Sarah L. Gaffen and Ashu Sharma J Immunol 2011; 187:501-509; Prepublished online 1 June 2011; doi: 10.4049/jimmunol.1100683 http://www.jimmunol.org/content/187/1/501 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2011/06/01/jimmunol.110068 Material 3.DC1 http://www.jimmunol.org/ References This article cites 62 articles, 24 of which you can access for free at: http://www.jimmunol.org/content/187/1/501.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on October 4, 2021 • Fast Publication! 4 weeks from acceptance to publication *average 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. The Journal of Immunology TLR2 Signaling and Th2 Responses Drive Tannerella forsythia-Induced Periodontal Bone Loss Srinivas R. Myneni,* Rajendra P. Settem,* Terry D. Connell,†,‡ Achsah D. Keegan,x Sarah L. Gaffen,{ and Ashu Sharma* Periodontal disease (PD) is a chronic inflammation of the tooth-supporting soft tissue and alveolar bone due to infection by a select group of Gram-negative microbes, which leads to tooth loss if untreated. Because mice deficient in CD4+ cells are resistant to infection-induced alveolar bone loss, Th cells have been implicated in bone-destructive processes during PD. However, the extent to which different Th cell subtypes play roles in pathogenesis or host protection remains to be defined and is likely to vary depending on the dominant microorganism involved. By far, Porphyromonas gingivalis is the best-studied periodontal microbe in PD. Although the Gram-negative anaerobe Tannerella forsythia is also a vital contributor to periodontal bone loss, almost nothing is known about immune responses to this organism. Previous studies from our laboratory revealed that T. forsythia induces Downloaded from periodontal bone loss in mice and that this bone loss depends on the bacterially expressed BspA protein. In this study, we showed that T. forsythia activates murine APCs primarily through TLR2-dependent signaling via BspA. Furthermore, T. forsythia in- fection causes a pronounced Th2 bias, evidenced by T cell expression of IL-5, but not IFN-g or IL-17, in draining lymph nodes. Consistently, deficiencies in TLR2 or STAT6 result in resistance to T. forsythia-induced alveolar bone loss. Thus, TLR2 signaling and Th2 cells play pathogenic roles in T. forsythia-induced alveolar bone destruction. The Journal of Immunology, 2011, 187: 501–509. http://www.jimmunol.org/ eriodontal disease (PD) is an inflammatory disease of the forsythia is a fastidious microbe with stringent growth require- tooth-supporting tissue (periodontium) that frequently ments. We were the first, to our knowledge, to document the vir- P leads to tooth loss (1) and is the most common cause of ulence potential of T. forsythia in a murine model of PD (9). In so inflammation-induced bone loss in humans. PD is caused by doing, we found that the alveolar bone loss is dependent on the a select group of anaerobic Gram-negative bacteria that colonize bacterially expressed virulence protein BspA (9). However, the subgingival spaces as biofilms. Periodontal bone destruction re- immune response to T. forsythia remains almost entirely undefined. sults mainly from the effects of the immune response to these Alveolar bone loss in response to oral infection by P. gingivalis biofilm bacteria (2, 3). The pathogenesis of PD is mediated by is dependent on the host response. For example, SCID mice or by guest on October 4, 2021 a polymicrobial consortium consisting of the Gram-negative mice specifically deficient in CD4+ T cells are resistant to alveolar pathogens Porphyromonas gingivalis, Treponema denticola, and bone loss due to P. gingivalis infection (10–12). Moreover, Th1 Tannerella forsythia, collectively known as the red complex (4–6). responses are associated with P. gingivalis-stimulated alveolar Although T. forsythia has been increasingly implicated in the bone loss in mice (13). In humans, the role of T cells in PD development and severity of PD, it remains a highly understudied pathobiology is complex, and data support a role for T cells in pathogen (7, 8). Its etiological role in PD has been recognized both protection and pathogenesis (6, 14–16). The existence of two relatively recently, and the virulence mechanisms of T. forsythia distinct effector CD4 T cell subsets has been recognized since are only just beginning to be defined (7). Unlike P. gingivalis, T. 1986 (17), with the description of Th1 (IFN-g–producing) and Th2 (IL-4-, IL-5- and IL-13–producing) cells. The Th17 lineage of IL-17–producing T cells was recognized in 2005 (18). In P. gin- *Department of Oral Biology, School of Dental Medicine, University at Buffalo, givalis infection, both Th1 and Th2 cytokines are found in the Buffalo, NY 14214; †Department of Microbiology and Immunology, University at Buffalo, Buffalo, NY 14214; ‡Witebsky Center for Microbial Pathogenesis and Im- periodontal lesion (6, 14–16). Prior to the discovery of Th17 cells, munology, University at Buffalo, Buffalo, NY 14214; xDepartment of Microbiology it was suggested that Th1 cells are characteristic of stable lesions, and Immunology, Center for Vascular and Inflammatory Diseases, University of whereas Th2 cells are associated with disease (14). However, IL- Maryland School of Medicine, Baltimore, MD 21201; and {Division of Rheumatol- ogy and Clinical Immunology, Department of Medicine, University of Pittsburgh, 17 was also documented in periodontitis patients with severe Pittsburgh, PA 15261 disease (19–22), and a significant number of CD4+ T cells isolated Received for publication March 8, 2011. Accepted for publication April 28, 2011. from gingival tissue of periodontitis patients express IL-17 (23). In This work was supported by U.S. Public Health R01 Grants DE1074905 (to A.S. P. gingivalis murine infections, IL-17 signaling is host protective and S.L.G.), DE14749 (to A.S.), DE13833 (to T.D.C.), and AI059775 and AI038985 by virtue of limiting infection via neutrophil mobilization (24). (to A.D.K.). The Th effector responses to T. forsythia are still poorly defined Address correspondence and reprint requests to Dr. Ashu Sharma, Department of and may be different from responses to P. gingivalis. This could Oral Biology, School of Dental Medicine, University at Buffalo, 311 Foster Hall, 3435 Main Street, Buffalo, NY 14214. E-mail address: [email protected] arise from differences in the nature of the pathogen-associated The online version of this article contains supplemental material. molecular patterns expressed on different periodontal pathogens, Abbreviations used in this article: ABC, alveolar bone crest; BMDC, bone marrow- which ultimately shape the adaptive response. In support of this derived dendritic cell; CEJ, cemento-enamel junction; cLN, cervical lymph node; notion, T. forsythia, unlike P. gingivalis, is unable to block neu- DC, dendritic cell; eLPS, Escherichia coli LPS; PD, periodontal disease; TRAP, trophil recruitment during infection in a mouse model (25), and tartrate-resistant acid phosphatase; WT, wild-type. recent studies demonstrated that T. forsythia, but not P. gingivalis, Copyright Ó 2011 by The American Association of Immunologists, Inc. 0022-1767/11/$16.00 preferentially activates TLR2. For instance, although P. gingivalis www.jimmunol.org/cgi/doi/10.4049/jimmunol.1100683 502 TLR2/Th2 RESPONSES DRIVE T. FORSYTHIA-INDUCED BONE LOSS through its fimbriae and LPS predominantly activate TLR2 (26), detected using HRP-conjugated goat anti-mouse IgG (Bethyl Laboratories, whole bacteria (27) and both minor and major fimbrial proteins Montgomery, TX). Specific serum IgG isotype Ab was detected by addition activate TLR4/CD14/MD2 (28, 29). Thus, the role of CD4 ef- of biotinylated isotype-specific secondary Ab (rat anti-mouse IgG1 or IgG2a; Southern Biotechnology, Birmingham, AL) followed by streptavidin- fector responses in PD bone loss remains poorly defined (14, 30), conjugated HRP (Southern Biotechnology). ELISA wells were color de- particularly specific responses to T. forsythia. veloped with TMB Microwell enzyme substrate (Kirkgaards and Perry, TLRs can play protective or destructive roles, depending on the Gaithersburg, MD). After stopping the enzyme reaction by adding 0.1 N nature of the invading pathogen and its associated virulence de- H2SO4, plates were read at 495 nm. The titer was defined as the log2 of the highest dilution with a signal that was 0.1 OD units above background. terminants (31). T. forsythia, as well as its virulence factor BspA, induce proinflammatory cytokine and chemokine secretion through Isolation of dendritic cells and macrophages and stimulation TLR2 (32–34). Signaling by TLR2 in APCs and expression of Bone marrow-derived dendritic cells (BMDCs) were generated as described specific cytokines were suggested to favor Th2 responses (35–38). (41). Briefly, femurs and tibias were flushed with PBS. Erythrocytes were Moreover, the Th2-specific transcription factor STAT6 was linked lysed using M-Lyse buffer (R&D Systems, Minneapolis, MN), and cells were to susceptibility to PD in mice (39). Accordingly, it was compelling suspended in RPMI 1640 supplemented with 10% heat-inactivated FCS, to determine the role of TLR2 and STAT6-mediated responses in T.
Load more

Recommended publications
  • Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease
    toxins Review Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease Rosalia Marcano 1, M. Ángeles Rojo 2 , Damián Cordoba-Diaz 3 and Manuel Garrosa 1,* 1 Department of Cell Biology, Histology and Pharmacology, Faculty of Medicine and INCYL, University of Valladolid, 47005 Valladolid, Spain; [email protected] 2 Area of Experimental Sciences, Miguel de Cervantes European University, 47012 Valladolid, Spain; [email protected] 3 Area of Pharmaceutics and Food Technology, Faculty of Pharmacy, and IUFI, Complutense University of Madrid, 28040 Madrid, Spain; [email protected] * Correspondence: [email protected] Abstract: It is widely recognized that periodontal disease is an inflammatory entity of infectious origin, in which the immune activation of the host leads to the destruction of the supporting tissues of the tooth. Periodontal pathogenic bacteria like Porphyromonas gingivalis, that belongs to the complex net of oral microflora, exhibits a toxicogenic potential by releasing endotoxins, which are the lipopolysaccharide component (LPS) available in the outer cell wall of Gram-negative bacteria. Endotoxins are released into the tissues causing damage after the cell is lysed. There are three well-defined regions in the LPS: one of them, the lipid A, has a lipidic nature, and the other two, the Core and the O-antigen, have a glycosidic nature, all of them with independent and synergistic functions. Lipid A is the “bioactive center” of LPS, responsible for its toxicity, and shows great variability along bacteria. In general, endotoxins have specific receptors at the cells, causing a wide immunoinflammatory response by inducing the release of pro-inflammatory cytokines and the production of matrix metalloproteinases.
    [Show full text]
  • Parents with Periodontitis Impact the Subgingival Colonization of Their Ofspring Mabelle Freitas Monteiro1, Khaled Altabtbaei2, Purnima S
    www.nature.com/scientificreports OPEN Parents with periodontitis impact the subgingival colonization of their ofspring Mabelle Freitas Monteiro1, Khaled Altabtbaei2, Purnima S. Kumar3,4*, Márcio Zafalon Casati1, Karina Gonzales Silverio Ruiz1, Enilson Antonio Sallum1, Francisco Humberto Nociti‑Junior1 & Renato Corrêa Viana Casarin1,4 Early acquisition of a pathogenic microbiota and the presence of dysbiosis in childhood is associated with susceptibility to and the familial aggregation of periodontitis. This longitudinal interventional case–control study aimed to evaluate the impact of parental periodontal disease on the acquisition of oral pathogens in their ofspring. Subgingival plaque and clinical periodontal metrics were collected from 18 parents with a history of generalized aggressive periodontitis and their children (6–12 years of age), and 18 periodontally healthy parents and their parents at baseline and following professional oral prophylaxis. 16S rRNA amplicon sequencing revealed that parents were the primary source of the child’s microbiome, afecting their microbial acquisition and diversity. Children of periodontitis parents were preferentially colonized by Filifactor alocis, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Streptococcus parasanguinis, Fusobacterium nucleatum and several species belonging to the genus Selenomonas even in the absence of periodontitis, and these species controlled inter‑bacterial interactions. These pathogens also emerged as robust discriminators of the microbial signatures of children of parents with periodontitis. Plaque control did not modulate this pathogenic pattern, attesting to the microbiome’s resistance to change once it has been established. This study highlights the critical role played by parental disease in microbial colonization patterns in their ofspring and the early acquisition of periodontitis‑related species and underscores the need for greater surveillance and preventive measures in families of periodontitis patients.
    [Show full text]
  • Treponema Pallidum, the Syphilis Spirochete: Making a Living As a Stealth Pathogen
    HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Nat Rev Manuscript Author Microbiol. Author Manuscript Author manuscript; available in PMC 2017 June 01. Published in final edited form as: Nat Rev Microbiol. 2016 December ; 14(12): 744–759. doi:10.1038/nrmicro.2016.141. Treponema pallidum, the syphilis spirochete: making a living as a stealth pathogen Justin D. Radolf1, Ranjit K. Deka2, Arvind Anand3, David Šmajs4, Michael V. Norgard5, and X. Frank Yang6 1Departments of Medicine, Pediatrics, Genetics and Genomic Science, Molecular Biology and Biophysics, and Immunology, UConn Health, Farmington, CT, USA 2Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, TX, USA 3Department of Medicine, UConn Health, Farmington, CT, USA 4Department of Biology, Faculty of Medicine, Masaryk University, Brno, Czech Republic 5Department of Microbiology, The University of Texas Southwestern Medical Center, Dallas, TX, USA 6Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN Abstract The last two decades have seen a worldwide resurgence in infections caused by Treponema pallidum subsp. pallidum, the syphilis spirochete. The syphilis spirochete’s well-recognized capacity for early dissemination and immune evasion has earned it the designation ‘the stealth pathogen’. Despite the many hurdles to studying syphilis pathogenesis, most notably the inability to culture and to genetically manipulate T. pallidum, in recent years, considerable progress has been made in elucidating the structural, physiologic, and regulatory facets of stealth pathogenicity. In this Review, we integrate this eclectic body of information to garner fresh insights into the highly successful parasitic lifestyles of the syphilis spirochete and related pathogenic treponemes. Pathogenic treponemes cause venereal syphilis, yaws, endemic syphilis, and pinta—multi- stage, infections that, although similar, can be differentiated based on clinical, epidemiologic, and geographic criteria1,2.
    [Show full text]
  • WHO GUIDELINES for the Treatment of Treponema Pallidum (Syphilis)
    WHO GUIDELINES FOR THE Treatment of Treponema pallidum (syphilis) WHO GUIDELINES FOR THE Treatment of Treponema pallidum (syphilis) WHO Library Cataloguing-in-Publication Data WHO guidelines for the treatment of Treponema pallidum (syphilis). Contents: Web annex D: Evidence profiles and evidence-to-decision frameworks - Web annex E: Systematic reviews for syphilis guidelines - Web annex F: Summary of conflicts of interest 1.Syphilis – drug therapy. 2.Treponema pallidum. 3.Sexually Transmitted Diseases. 4.Guideline. I.World Health Organization. ISBN 978 92 4 154980 6 (NLM classification: WC 170) © World Health Organization 2016 All rights reserved. Publications of the World Health Organization are available on the WHO website (http://www.who.int) or can be purchased from WHO Press, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel.: +41 22 791 3264; fax: +41 22 791 4857; email: [email protected]). Requests for permission to reproduce or translate WHO publications – whether for sale or for non-commercial distribution– should be addressed to WHO Press through the WHO website (http://www.who.int/about/licensing/ copyright_form/index.html). The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted and dashed lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned.
    [Show full text]
  • The Role of Porphyromonas Gingivalis Virulence Factors in Periodontitis Immunopathogenesis
    The Role of Porphyromonas gingivalis Virulence Factors in Periodontitis Immunopathogenesis (Peran Faktor Virulensi Porphyromonas Gingivalis pada Imunopatogenesis Periodontitis) Tienneke Riana Septiwidyati, Endang Winiati Bachtiar Department of Oral Biology, Faculty of Dentistry, Universitas Indonesia, Jakarta, Indonesia, Email: [email protected] Abstract Porphyromonas gingivalis is an anaerobic Gram-negative bacteria, often associated with the pathogenesis of periodontitis. Periodontitis is a chronic inflammation characterized by damage to the supporting tissues of the tooth. Porphyromonas gingivalis locally can invade periodontal tissue and avoid host defence mechanisms. Porphyromonas gingivalis have virulence factors that can interfere with host immune response and cause inflammation at host tissue. The aim of this article is to provide an overview of the role of Porphyromonas gingivalis virulence factors such as capsules, fimbriae, lipopolysaccharides, and gingipain in the pathogenesis of periodontitis. The data sources were taken from PubMed and Google Scholar within 10 years. The role of Porphyromonas gingivalis capsule is to suppress the host's immune response to bacteria by reducing phagocytosis so the bacteria can survive. The roles of Porphyromonas gingivalis fimbriaeare to facilitate adhesion and invasion of bacteria to host cells so the damage will occur in the periodontal tissue. One of the roles of Porphyromoas gingivalis lipopolysaccharide is to disrupt the host immune system by disrupting the distribution of leukocytes around bacterial colonization so the bacteria can survive. The role of the Porphyromonas gingivalis gingipain is to suppress inflammatory cytokines thereby reducing the host's response by manipulating the complement system and disrupting the response of T cells. Porphyromonas gingivalis expresses several virulence factors involved in the colonization of subgingival plaque, modulates the immune response of host cells, and damages the host tissue directly so it can cause periodontitis.
    [Show full text]
  • Periodontal, Metabolic, and Cardiovascular Disease
    Pteridines 2018; 29: 124–163 Research Article Open Access Hina Makkar, Mark A. Reynolds#, Abhishek Wadhawan, Aline Dagdag, Anwar T. Merchant#, Teodor T. Postolache*# Periodontal, metabolic, and cardiovascular disease: Exploring the role of inflammation and mental health Journal xyz 2017; 1 (2): 122–135 The First Decade (1964-1972) https://doi.org/10.1515/pteridines-2018-0013 receivedResearch September Article 13, 2018; accepted October 10, 2018. List of abbreviations Abstract: Previous evidence connects periodontal AAP: American Academy of Periodontology Max Musterman, Paul Placeholder disease, a modifiable condition affecting a majority of AGEs: Advanced glycation end products Americans,What withIs So metabolic Different and cardiovascular About morbidity AgP: Aggressive periodontitis and mortality. This review focuses on the likely mediation AHA: American Heart Association ofNeuroenhancement? these associations by immune activation and their anti-CL: Anti-cardiolipin potentialWas istinteractions so anders with mental am Neuroenhancement?illness. Future anti-oxLDL: Anti-oxidized low-density lipoprotein longitudinal, and ideally interventional studies, should AP: Acute periodontitis focus on reciprocal interactions and cascading effects, as ASCVD: Atherosclerotic cardiovascular disease wellPharmacological as points for effective and Mentalpreventative Self-transformation and therapeutic C. pneumoniae in Ethic : Chlamydia pneumoniae interventionsComparison across diagnostic domains to reduce CAL: Clinical attachment loss morbidity,Pharmakologische
    [Show full text]
  • Morphology of Spirochaeta Myelophthora in Multiple Sclerosis
    MORPHOLOGY OF SPIROCHAETA MYELOPHTHORA IN MULTIPLE SCLEROSIS GABRIEL STEINER, M.D. (Detroit, Mich.) In a recent paper (1) the findings of specific spirochetes in the brain of a newly examined subacute case of multiple sclerosis were reported and evaluated. The purpose of the present paper is to give a detailed description of these spiro­ chetes, their classification, their reproduction, and disintegration. Four cases of multiple sclerosis, including the case to be reported, elicited abundant numbers of specific spirochetes in the central nervous system to war­ rant the publication of this paper. Downloaded from 1. Further Evidence of Spirochetal Nature: It has been said that the reported spirochetes represent only spirochete-like structures of the tissue proper, such as reticulin fibrils, neurofibrils, or axis cylinders.* To disprove these objections the following experiments were done: Sections from brains of general paresis containing numerous spirochetes in the cortex and those from lungs in congenital syphilis were stained with my silver technique II (1), then desilverized with potassium permanganate and oxalic acid (A. J. Wilson (2)), http://jnen.oxfordjournals.org/ and restained for reticulin fibers (Wilder's method). They showed clearly the complete absence of spirochetes in these restained sections, at regions where many spirochetes were formerly seen. Reticulin fibrils were easily demonstrable. Such sections could be desilverized again and restained for spirochetes with positive results. In sections stained for axis cylin­ ders (Bielschowsky's axis cylinder method for paraffin sections), no spirochetes were seen in places where previously masses of treponemas were present. Desilverizing and restaining with technique II brought the spirochetes out again.
    [Show full text]
  • Peri-Implantitis Review a Quarterly Review of the Latest Publications Related to the Study of Peri-Implant Inflammation and Bone Loss
    12 Fall 2015 Aron J. Saffer DDS MS Diplomate of the American Board of Periodontology Peri-implantitis Review A quarterly review of the latest publications related to the study of Peri-implant inflammation and bone loss A service of Dr. Aron Saffer and the Jerusalem Perio Center to provide useful, up -to date information concerning one of the most complex and troubling problems facing dental professionals today. Peri-implantitis : Microbiology • Are the Bacteria of Peri-implantitis the same as Periodontal disease? • Are we treating the infection correctly? MICROBIAL METHODS EMPLOYED • Are screw-retained restorations better than cement IN THE DIAGNOSIS OF THE retained restorations at preventing peri-implantitis PERIODONTAL PATHOGEN: Bacterial Cultivation: a method in What Does the latest Literature say? You might be surprised which the bacteria taken from infected site and is allowed to multiply on a predetermined culture media. Using light Peri-implant mucositis and Peri-implantitis is an inflammatory response microscopy the bacteria is generally due to bacteriorly driven infections, affecting the mucosal tissue and identified. eventually the bone surrounding implants. The condition was traditionally regarded to be microbiologically similar to Periodontitis. Earlier research had demonstrated that the pathogens which were found in patients with periodontal disease had similar pathogens in the sulcus around infected implants. In fact, one hypothesis suggested that the infected gingiva was a resevoir for the bacteria that would eventually translocate and infect the mucosal crevice around implants. With newer microbiological identification techniques evidence is emerging . to suggest that the ecosystem around teeth and implants differ in many ways. Have we been taking “the easy way out” by lumping ALL gingival and mucosal infection together regardless whether it surrounds a human tooth or titanium metal.
    [Show full text]
  • Downloaded from 3
    Philips et al. BMC Genomics (2020) 21:402 https://doi.org/10.1186/s12864-020-06810-9 RESEARCH ARTICLE Open Access Analysis of oral microbiome from fossil human remains revealed the significant differences in virulence factors of modern and ancient Tannerella forsythia Anna Philips1, Ireneusz Stolarek1, Luiza Handschuh1, Katarzyna Nowis1, Anna Juras2, Dawid Trzciński2, Wioletta Nowaczewska3, Anna Wrzesińska4, Jan Potempa5,6 and Marek Figlerowicz1,7* Abstract Background: Recent advances in the next-generation sequencing (NGS) allowed the metagenomic analyses of DNA from many different environments and sources, including thousands of years old skeletal remains. It has been shown that most of the DNA extracted from ancient samples is microbial. There are several reports demonstrating that the considerable fraction of extracted DNA belonged to the bacteria accompanying the studied individuals before their death. Results: In this study we scanned 344 microbiomes from 1000- and 2000- year-old human teeth. The datasets originated from our previous studies on human ancient DNA (aDNA) and on microbial DNA accompanying human remains. We previously noticed that in many samples infection-related species have been identified, among them Tannerella forsythia, one of the most prevalent oral human pathogens. Samples containing sufficient amount of T. forsythia aDNA for a complete genome assembly were selected for thorough analyses. We confirmed that the T. forsythia-containing samples have higher amounts of the periodontitis-associated species than the control samples. Despites, other pathogens-derived aDNA was found in the tested samples it was too fragmented and damaged to allow any reasonable reconstruction of these bacteria genomes. The anthropological examination of ancient skulls from which the T.
    [Show full text]
  • Cigarette Smoke Promotes Genomic Evolution in the Periodontal Pathogen Porphyromonas Gingivalis
    University of Louisville ThinkIR: The University of Louisville's Institutional Repository Electronic Theses and Dissertations 5-2013 Cigarette smoke promotes genomic evolution in the periodontal pathogen Porphyromonas gingivalis. Josh George University of Louisville Follow this and additional works at: https://ir.library.louisville.edu/etd Recommended Citation George, Josh, "Cigarette smoke promotes genomic evolution in the periodontal pathogen Porphyromonas gingivalis." (2013). Electronic Theses and Dissertations. Paper 486. https://doi.org/10.18297/etd/486 This Master's Thesis is brought to you for free and open access by ThinkIR: The University of Louisville's Institutional Repository. It has been accepted for inclusion in Electronic Theses and Dissertations by an authorized administrator of ThinkIR: The University of Louisville's Institutional Repository. This title appears here courtesy of the author, who has retained all other copyrights. For more information, please contact [email protected]. CIGARETTE SMOKE PROMOTES GENOMIC EVOLUTION IN THE PERIODONTAL PATHOGEN PORPHYROMONAS GINGIVALIS by JOSH GEORGE B.S. Biology A Thesis Submitted to the Faculty of the School of Dentistry of the University of Louisville In Partial Fulfillment of the Requirements For the Degree of Master of Science Oral Biology University of Louisville Louisville, Kentucky May 2013 CIGARETTE SMOKE PROMOTES GENOMIC EVOLUTION IN THE PERIODONTAL PATHOGEN PORPHYROMONAS GINGIVALIS by JOSH GEORGE B.S. Biology A Thesis Approved on April 26, 2013 By the following Thesis Committee: ________________________________________________________ David Scott Ph.D. – Mentor/Director _______________________________________________________ Ted Kalbfleisch Ph.D. – Committee Member _______________________________________________________ Jan Potempa Ph.D. – Committee Member _______________________________________________________ Don Demuth Ph.D. – Committee Member ii ACKNOWLEDGMENTS I would like to thank Dr.
    [Show full text]
  • Exploring Salivary Microbiota in AIDS Patients with Different Periodontal Statuses Using 454 GS-FLX Titanium Pyrosequencing
    ORIGINAL RESEARCH published: 02 July 2015 doi: 10.3389/fcimb.2015.00055 Exploring salivary microbiota in AIDS patients with different periodontal statuses using 454 GS-FLX Titanium pyrosequencing Fang Zhang 1 †, Shenghua He 2 †, Jieqi Jin 1, Guangyan Dong 1 and Hongkun Wu 3* 1 State Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China, 2 Public Health Clinical Center of Chengdu, Chengdu, China, 3 Department of Geriatric Dentistry, West China College of Stomatology, Sichuan University, Chengdu, China Patients with acquired immunodeficiency syndrome (AIDS) are at high risk of opportunistic infections. Oral manifestations have been associated with the level of immunosuppression, these include periodontal diseases, and understanding the microbial populations in the oral cavity is crucial for clinical management. The aim of this study was to examine the salivary bacterial diversity in patients newly admitted to the AIDS ward of the Public Health Clinical Center (China). Saliva samples were Edited by: Saleh A. Naser, collected from 15 patients with AIDS who were randomly recruited between December University of Central Florida, USA 2013 and March 2014. Extracted DNA was used as template to amplify bacterial Reviewed by: 16S rRNA. Sequencing of the amplicon library was performed using a 454 GS-FLX J. Christopher Fenno, University of Michigan, USA Titanium sequencing platform. Reads were optimized and clustered into operational Nick Stephen Jakubovics, taxonomic units for further analysis. A total of 10 bacterial phyla (106 genera) were Newcastle University, UK detected. Firmicutes, Bacteroidetes, and Proteobacteria were preponderant in the *Correspondence: salivary microbiota in AIDS patients. The pathogen, Capnocytophaga sp., and others Hongkun Wu, Department of Geriatric Dentistry, not considered pathogenic such as Neisseria elongata, Streptococcus mitis, and West China College of Stomatology, Mycoplasma salivarium but which may be opportunistic infective agents were detected.
    [Show full text]
  • Oral Microbiota Features in Subjects with Down Syndrome and Periodontal Diseases: a Systematic Review
    International Journal of Molecular Sciences Review Oral Microbiota Features in Subjects with Down Syndrome and Periodontal Diseases: A Systematic Review Maria Contaldo 1,* , Alberta Lucchese 1, Antonio Romano 1 , Fedora Della Vella 2 , Dario Di Stasio 1 , Rosario Serpico 1 and Massimo Petruzzi 2 1 Multidisciplinary Department of Medical-Surgical and Dental Specialties, University of Campania Luigi Vanvitelli, Via Luigi de Crecchio, 6, 80138 Naples, Italy; [email protected] (A.L.); [email protected] (A.R.); [email protected] (D.D.S.); [email protected] (R.S.) 2 Interdisciplinary Department of Medicine, University of Bari “Aldo Moro”, 70121 Bari, Italy; [email protected] (F.D.V.); [email protected] (M.P.) * Correspondence: [email protected] or [email protected]; Tel.: +39-3204876058 Abstract: Down syndrome (DS) is a genetic disorder associated with early-onset periodontitis and other periodontal diseases (PDs). The present work aimed to systematically review the scientific literature reporting studies in vivo on oral microbiota features in subjects with DS and related periodontal health and to highlight any correlation and difference with subjects not affected by DS, with and without PDs. PubMed, Web of Science, Scopus and Cochrane were searched for relevant studies in May 2021. The participants were subjects affected by Down syndrome (DS) with and without periodontal diseases; the study compared subjects with periodontal diseases but not affected by DS, and DS without periodontal diseases; the outcomes were the differences in oral microbiota/periodontopathogen bacterial composition among subjects considered; the study Citation: Contaldo, M.; Lucchese, A.; design was a systematic review.
    [Show full text]