Interleukin-17A is required to suppress invasion of Salmonella enterica serovar Typhimurium to enteric mucosa.
Immunology
; 131(3): 377-85, 2010 Nov.
Article
em En
| MEDLINE
| ID: mdl-20575990
ABSTRACT
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 ß-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.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Salmonella typhi
/
Febre Tifoide
/
Células Th1
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Interleucina-17
/
Mucosa Intestinal
Limite:
Animals
Idioma:
En
Ano de publicação:
2010
Tipo de documento:
Article