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dc.contributor.authorSuwandi, Abdulhadi
dc.contributor.authorBargen, Imke
dc.contributor.authorPils, Marina C
dc.contributor.authorKrey, Martina
dc.contributor.authorZur Lage, Susanne
dc.contributor.authorSingh, Anurag K
dc.contributor.authorBasler, Tina
dc.contributor.authorFalk, Christine S
dc.contributor.authorSeidler, Ursula
dc.contributor.authorHornef, Mathias W
dc.contributor.authorGoethe, Ralph
dc.contributor.authorWeiss, Siegfried
dc.date.accessioned2017-04-12T14:43:10Z
dc.date.available2017-04-12T14:43:10Z
dc.date.issued2017
dc.identifier.citationCD4 T Cell Dependent Colitis Exacerbation Following Re-Exposure of Mycobacterium avium ssp. paratuberculosis. 2017, 7:75 Front Cell Infect Microbiolen
dc.identifier.issn2235-2988
dc.identifier.pmid28361039
dc.identifier.doi110.1097/MIB.0000000000000157
dc.identifier.urihttp://hdl.handle.net/10033/620895
dc.description.abstractMycobacterium avium ssp. paratuberculosis (MAP) is the causative agent of Johne's disease (JD), a chronic inflammatory bowel disease of cattle characterized by intermittent to chronic diarrhea. In addition, MAP has been isolated from Crohn's disease (CD) patients. The impact of MAP on severity of clinical symptoms in JD as well as its role in CD are yet unknown. We have previously shown that MAP is able to colonize inflamed enteric tissue and to exacerbate the inflammatory tissue response (Suwandi et al., 2014). In the present study, we analyzed how repeated MAP administration influences the course of dextran sulfate sodium (DSS)-induced colitis. In comparison to mice exposed to DSS or MAP only, repeated exposure of DSS-treated mice to MAP (DSS/MAP) revealed a significantly enhanced clinical score, reduction of colon length as well as severe CD4(+) T cell infiltration into the colonic lamina propria. Functional analysis identified a critical role of CD4(+) T cells in the MAP-induced disease exacerbation. Additionally, altered immune responses were observed when closely related mycobacteria species such as M. avium ssp. avium and M. avium ssp. hominissuis were administered. These data reveal the specific ability of MAP to aggravate intestinal inflammation and clinical symptoms. Overall, this phenotype is compatible with similar disease promoting capabilites of MAP in JD and CD.
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.titleCD4 T Cell Dependent Colitis Exacerbation Following Re-Exposure of Mycobacterium avium ssp. paratuberculosis.en
dc.typeArticleen
dc.contributor.departmentHelmholtz Centre for infection research, Inhoffenstr.7, 38124 Braunschweig, Germany.en
dc.identifier.journalFrontiers in cellular and infection microbiologyen
refterms.dateFOA2018-06-13T00:12:59Z
html.description.abstractMycobacterium avium ssp. paratuberculosis (MAP) is the causative agent of Johne's disease (JD), a chronic inflammatory bowel disease of cattle characterized by intermittent to chronic diarrhea. In addition, MAP has been isolated from Crohn's disease (CD) patients. The impact of MAP on severity of clinical symptoms in JD as well as its role in CD are yet unknown. We have previously shown that MAP is able to colonize inflamed enteric tissue and to exacerbate the inflammatory tissue response (Suwandi et al., 2014). In the present study, we analyzed how repeated MAP administration influences the course of dextran sulfate sodium (DSS)-induced colitis. In comparison to mice exposed to DSS or MAP only, repeated exposure of DSS-treated mice to MAP (DSS/MAP) revealed a significantly enhanced clinical score, reduction of colon length as well as severe CD4(+) T cell infiltration into the colonic lamina propria. Functional analysis identified a critical role of CD4(+) T cells in the MAP-induced disease exacerbation. Additionally, altered immune responses were observed when closely related mycobacteria species such as M. avium ssp. avium and M. avium ssp. hominissuis were administered. These data reveal the specific ability of MAP to aggravate intestinal inflammation and clinical symptoms. Overall, this phenotype is compatible with similar disease promoting capabilites of MAP in JD and CD.


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