Abstract:
:Citrobacter rodentium, a murine model pathogen for enteropathogenic Escherichia coli, colonizes the surface of intestinal epithelial cells and causes mucosal inflammation. This bacterium is an ideal model for investigating pathogen-host immune interactions in the gut. It is well known that gene transcripts for Th1 cytokines are highly induced in colonic tissue from mice infected with C. rodentium. However, it remains to be seen whether the Th1 or Th2 cytokines produced by antigen-specific CD4(+) T cells provide effective regulation of the host immune defense against C. rodentium infection. To investigate the antigen-specific immune responses, C. rodentium expressing ovalbumin (OVA-C. rodentium), a model antigen, was generated and used to define antigen-specific responses under gamma interferon (IFN-gamma)-deficient or interleukin-4 (IL-4)-deficient conditions in vivo. The activation of antigen-specific CD4(+) T cells and macrophage phagocytosis were evaluated in the presence of IFN-gamma or IL-4 in vitro. IFN-gamma-deficient mice exhibited a loss of body weight and a higher bacterial concentration in feces during OVA-C. rodentium infection than C57BL/6 (wild type) or IL-4-deficient mice. This occurred through the decreased efficiency of macrophage phagocytosis and the activation of antigen-specific CD4(+) T cells. Furthermore, a deficiency in antigen-specific CD4(+) T-cell-expressed IFN-gamma led to a higher susceptibility to mucosal and gut-derived systemic OVA-C. rodentium infection. These results show that the IFN-gamma produced by antigen-specific CD4(+) T cells plays an important role in the defense against C. rodentium.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
Shiomi H,Masuda A,Nishiumi S,Nishida M,Takagawa T,Shiomi Y,Kutsumi H,Blumberg RS,Azuma T,Yoshida Mdoi
10.1128/IAI.01343-09subject
Has Abstractpub_date
2010-06-01 00:00:00pages
2653-66issue
6eissn
0019-9567issn
1098-5522pii
IAI.01343-09journal_volume
78pub_type
杂志文章abstract::Inactivation of sortase gene srtA in Streptococcus pneumoniae strain R6 caused the release of beta-galactosidase and neuraminidase A (NanA) from the cell wall into the surrounding medium. Both of these surface proteins contain the LPXTG motif in the C-terminal domain. Complementation with plasmid-borne srtA reversed p...
journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
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journal_title:Infection and immunity
pub_type: 杂志文章
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journal_title:Infection and immunity
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pub_type: 杂志文章
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journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.66.10.4856-4866.1998
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journal_title:Infection and immunity
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doi:10.1128/IAI.6.2.119-126.1972
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journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.20.3.728-731.1978
更新日期:1978-06-01 00:00:00
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pub_type: 杂志文章
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journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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pub_type: 杂志文章
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journal_title:Infection and immunity
pub_type: 杂志文章
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