Source:http://linkedlifedata.com/resource/pubmed/id/20575990
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2010-11-2
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pubmed:abstractText |
Salmonella enterica serovar Typhimurium (S. typhimurium) causes a localized enteric infection and its elimination is dependent on a T helper type 1 immune response. However, the mechanism of the protective immune response against the pathogen in gut-associated lymphoid tissue (GALT) at an early stage of the infection is not yet clarified. Here, we show that interleukin-17A (IL-17A) was constitutively expressed in GALT; it was also detected on crypt and epithelial cells of the small intestine. Neutralization of the IL-17A in the intestinal lumen exacerbated epithelial damage induced by intestinal S. typhimurium infection at an early stage of the infection. The result suggests that IL-17A has a pivotal role in the immediate early stage of protection against bacterial infection at the intestinal mucosa. As IL-17A neutralization also suppressed the constitutive localization of ?-defensin 3 (BD3), an IL-17A-induced antimicrobial peptide, at the apical site of the intestinal mucosa, it is estimated that IL-17A constitutively induces the expression of the antimicrobial peptide to kill invading pathogens at the epithelial surface immediately after the infection. In contrast, interferon-? is induced around 3 days after S. typhimurium infection, and its expression level increases thereafter. Taken together, the findings lead to the hypothesis that IL-17A participates in the immediate early stage of protection against S. typhimurium intestinal infection whereas interferon-? is important at a later stage of the infection.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Blocking,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-17,
http://linkedlifedata.com/resource/pubmed/chemical/beta-Defensins,
http://linkedlifedata.com/resource/pubmed/chemical/beta-defensin 3, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1365-2567
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pubmed:author | |
pubmed:copyrightInfo |
© 2010 The Authors. Immunology © 2010 Blackwell Publishing Ltd.
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pubmed:issnType |
Electronic
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pubmed:volume |
131
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
377-85
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pubmed:dateRevised |
2011-11-1
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pubmed:meshHeading |
pubmed-meshheading:20575990-Animals,
pubmed-meshheading:20575990-Antibodies, Blocking,
pubmed-meshheading:20575990-Immunity, Mucosal,
pubmed-meshheading:20575990-Interferon-gamma,
pubmed-meshheading:20575990-Interleukin-17,
pubmed-meshheading:20575990-Intestinal Mucosa,
pubmed-meshheading:20575990-Intestine, Small,
pubmed-meshheading:20575990-Male,
pubmed-meshheading:20575990-Mice,
pubmed-meshheading:20575990-Mice, Inbred C57BL,
pubmed-meshheading:20575990-Salmonella typhi,
pubmed-meshheading:20575990-Th1 Cells,
pubmed-meshheading:20575990-Typhoid Fever,
pubmed-meshheading:20575990-beta-Defensins
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pubmed:year |
2010
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pubmed:articleTitle |
Interleukin-17A is required to suppress invasion of Salmonella enterica serovar Typhimurium to enteric mucosa.
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pubmed:affiliation |
Center of Molecular Biosciences, Tropical Biosphere Research Centre, University of the Ryukyus, Senbaru, Nishihara, Okinawa, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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