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      Clostridioides difficile Binary Toxin Is Recognized by the Toll-Like Receptor 2/6 Heterodimer to Induce a Nuclear Factor-κB Response

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          Abstract

          Clostridioides difficile infection (CDI) represents a significant burden on the health care system, one that is exacerbated by the emergence of binary toxin (CDT)-producing hypervirulent C. difficile strains. Previous work from our laboratory has shown that Toll-like receptor 2 (TLR2) recognizes CDT to induce inflammation. Here we explore the interactions of CDT with TLR2 and the impact on host immunity during CDI. We found that the TLR2/6 heterodimer, not TLR2/1, is responsible for CDT recognition, and that gene pathways including nuclear factor-κB and MAPK downstream of TLR2/6 are upregulated in mice with intact TLR2/6 signaling during CDI.

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          Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2

          Michael Love, Wolfgang Huber, Simon Anders (2014)
          In comparative high-throughput sequencing assays, a fundamental task is the analysis of count data, such as read counts per gene in RNA-seq, for evidence of systematic changes across experimental conditions. Small replicate numbers, discreteness, large dynamic range and the presence of outliers require a suitable statistical approach. We present DESeq2, a method for differential analysis of count data, using shrinkage estimation for dispersions and fold changes to improve stability and interpretability of estimates. This enables a more quantitative analysis focused on the strength rather than the mere presence of differential expression. The DESeq2 package is available at http://www.bioconductor.org/packages/release/bioc/html/DESeq2.html. Electronic supplementary material The online version of this article (doi:10.1186/s13059-014-0550-8) contains supplementary material, which is available to authorized users.
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            Burden ofClostridium difficileInfection in the United States

            Fernanda Lessa, Yi Mu, Wendy Bamberg … (2015)
            The magnitude and scope of Clostridium difficile infection in the United States continue to evolve.
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              The Role of TLR2 in Infection and Immunity

              Laura Oliveira-Nascimento, Paola Massari, Lee M. Wetzler (2012)
              Toll-like receptors (TLRs) are recognition molecules for multiple pathogens, including bacteria, viruses, fungi, and parasites. TLR2 forms heterodimers with TLR1 and TLR6, which is the initial step in a cascade of events leading to significant innate immune responses, development of adaptive immunity to pathogens and protection from immune sequelae related to infection with these pathogens. This review will discuss the current status of TLR2 mediated immune responses by recognition of pathogen-associated molecular patterns (PAMPS) on these organisms. We will emphasize both canonical and non-canonical responses to TLR2 ligands with emphasis on whether the inflammation induced by these responses contributes to the disease state or to protection from diseases.
              Article 0 comments Cited 229 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Infect Dis
                Journal ID (iso-abbrev): J Infect Dis
                Journal ID (publisher-id): jid
                Title: The Journal of Infectious Diseases
                Publisher: Oxford University Press (US )
                ISSN (Print): 0022-1899
                ISSN (Electronic): 1537-6613
                Publication date Collection: 01 April 2022
                Publication date (Electronic): 03 October 2020
                Publication date PMC-release: 03 October 2020
                Volume: 225
                Issue: 7
                Pages: 1296-1300
                Affiliations
                [1 ] Department of Pathology, University of Virginia , Charlottesville, Virginia, USA
                [2 ] Department of Microbiology, Immunology, and Cancer Biology, University of Virginia , Charlottesville, Virginia, USA
                [3 ] Department of Biochemistry and Molecular Genetics, University of Virginia , Charlottesville, Virginia, USA
                [4 ] Institute of Experimental and Clinical Pharmacology and Toxicology, Faculty of Medicine, University of Freiburg , Freiburg, Germany
                [5 ] Department of Medicine, University of Virginia , Charlottesville, Virginia, USA
                Author notes
                Correspondence: William Petri Jr, MD, PhD, PO Box 801340, Charlottesville, VA 22908-1340 ( wap3g@ 123456virginia.edu ).
                Article
                Publisher ID: jiaa620
                DOI: 10.1093/infdis/jiaa620
                PMC ID: 8974845
                PubMed ID: 33011801
                SO-VID: d9069645-070c-4017-b355-cd11be13b975
                Copyright © © The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence ( https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                Date received : 01 June 2020
                Date: 24 September 2020
                Date accepted : 29 September 2020
                Date: 21 November 2020
                Page count
                Pages: 5
                Funding
                Funded by: National Institute of Allergy and Infectious Diseases, DOI 10.13039/100000060;
                Award ID: R01 AI124214
                Award ID: T32AI007496
                Categories
                Subject: Major Articles and Brief Reports
                Subject: Pathogenesis and Host Response
                Subject: AcademicSubjects/MED00290

                ScienceOpen disciplines: Infectious disease & Microbiology
                Keywords: clostridioides difficile,cdt,binary toxin,immune response,innate immunity,tlr2,tlr6,nf-κb
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology
                Keywords: clostridioides difficile, cdt, binary toxin, immune response, innate immunity, tlr2, tlr6, nf-κb

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