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Interleukin‐17A is required to suppress invasion of Salmonella enterica serovar Typhimurium to enteric mucosa
Author(s) -
Mayuzumi Hirokazu,
InagakiOhara Kyoko,
Uyttenhove Catherine,
Okamoto Yuko,
Matsuzaki Goro
Publication year - 2010
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2010.03310.x
Subject(s) - salmonella enterica , biology , microbiology and biotechnology , salmonella , intestinal mucosa , immune system , pathogen , salmonella infection , enteric virus , intestinal epithelium , enterobacteriaceae , antimicrobial peptides , antimicrobial , immunity , epithelium , immunology , bacteria , escherichia coli , gene , medicine , biochemistry , genetics
Summary 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 β‐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‐γ 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‐γ is important at a later stage of the infection.