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    Analysis of the Human Mucosal Response to Cholera Reveals Sustained Activation of Innate Immune Signaling Pathways

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    Authors
    Bourque, Daniel L.
    Genereux, Diane P.
    Karlsson, Elinor K.
    Qadri, Firdausi
    Harris, Jason B.
    UMass Chan Affiliations
    Program in Bioinformatics and Integrative Biology
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2018-01-22
    Keywords
    Vibrio cholerae
    immune mechanisms
    mucosal immunity
    Bacterial Infections and Mycoses
    Bioinformatics
    Computational Biology
    Genetics and Genomics
    Immunity
    Immunology of Infectious Disease
    
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    Abstract
    To better understand the innate immune response to Vibrio cholerae infection, we tracked gene expression in the duodenal mucosa of 11 Bangladeshi adults with cholera, using biopsy specimens obtained immediately after rehydration and 30 and 180 days later. We identified differentially expressed genes and performed an analysis to predict differentially regulated pathways and upstream regulators. During acute cholera, there was a broad increase in the expression of genes associated with innate immunity, including activation of the NF-kappaB, mitogen-activated protein kinase (MAPK), and Toll-like receptor (TLR)-mediated signaling pathways, which, unexpectedly, persisted even 30 days after infection. Focusing on early differences in gene expression, we identified 37 genes that were differentially expressed on days 2 and 30 across the 11 participants. These genes included the endosomal Toll-like receptor gene TLR8, which was expressed in lamina propria cells. Underscoring a potential role for endosomal TLR-mediated signaling in vivo, our pathway analysis found that interferon regulatory factor 7 and beta 1 and alpha 2 interferons were among the top upstream regulators activated during cholera. Among the innate immune effectors, we found that the gene for DUOX2, an NADPH oxidase involved in the maintenance of intestinal homeostasis, was upregulated in intestinal epithelial cells during cholera. Notably, the observed increases in DUOX2 and TLR8 expression were also modeled in vitro when Caco-2 or THP-1 cells, respectively, were stimulated with live V. cholerae but not with heat-killed organisms or cholera toxin alone. These previously unidentified features of the innate immune response to V. cholerae extend our understanding of the mucosal immune signaling pathways and effectors activated in vivo following cholera.
    Source

    Infect Immun. 2018 Jan 22;86(2). pii: e00594-17. doi: 10.1128/IAI.00594-17. Print 2018 Feb. Link to article on publisher's site

    DOI
    10.1128/IAI.00594-17
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/25848
    PubMed ID
    29133347
    Notes

    Full author list omitted for brevity. For the full list of authors, see article.

    Related Resources

    Link to Article in PubMed

    Rights
    Copyright © 2018, American Society for Microbiology. Publisher PDF posted as allowed by the publisher's copyright policy at https://journals.asm.org/content/copyright-transfer-and-supplemental-material-license-agreement-2017.
    ae974a485f413a2113503eed53cd6c53
    10.1128/IAI.00594-17
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    Program in Bioinformatics and Integrative Biology Publications

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