ovalbumin and Enterobacteriaceae-Infections

Up to 20% of people worldwide develop gastrointestinal symptoms following a meal

Topics: Abdominal Pain; Adult; Allergens; Animals; Citrobacter rodentium; Diarrhea; Enterobacteriaceae Infections; Female; Food; Food Hypersensitivity; Glutens; Humans; Immunoglobulin E; Intestinal Mucosa; Intestines; Irritable Bowel Syndrome; Male; Mast Cells; Mice; Mice, Inbred BALB C; Middle Aged; Milk; Ovalbumin; Quality of Life; Receptors, Histamine H1; Soybean Proteins; Triticum

Topics: Abdominal Pain; Animals; Citrobacter rodentium; Disease Models, Animal; Enterobacteriaceae Infections; Food Hypersensitivity; Humans; Immunoglobulin E; Irritable Bowel Syndrome; Mast Cells; Mice; Ovalbumin

The interleukin-17 (IL-17) family of cytokines has emerged as a critical player in inflammatory diseases. Among them, IL-25 has been shown to be important in allergic inflammation and protection against parasitic infection. Here we have demonstrated that IL-17B, a poorly understood cytokine, functions to inhibit IL-25-driven inflammation. IL-17B and IL-25, both binding to the interleukin-17 receptor B (IL-17RB), were upregulated in their expression after acute colonic inflammation. Individual inhibition of these cytokines revealed opposing functions in colon inflammation: IL-25 was pathogenic but IL-17B was protective. Similarly opposing phenotypes were observed in Citrobacter rodentium infection and allergic asthma. Moreover, IL-25 was found to promote IL-6 production from colon epithelial cells, which was inhibited by IL-17B. Therefore, our data demonstrate that IL-17B is an anti-inflammatory cytokine in the IL-17 family.

Topics: Animals; Anti-Bacterial Agents; Asthma; Cell Line; Citrobacter rodentium; Colitis; Dysbiosis; Enterobacteriaceae Infections; Epithelial Cells; Gene Expression Regulation; Interleukin-17; Interleukin-6; Interleukins; Intestinal Mucosa; Mice; Mice, Inbred C57BL; Mice, Knockout; Ovalbumin; Protein Binding; Receptors, Interleukin-17; Signal Transduction; Sodium Dodecyl Sulfate

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.

Topics: Animals; Body Weight; CD4-Positive T-Lymphocytes; Cells, Cultured; Citrobacter rodentium; Enterobacteriaceae Infections; Feces; Female; Immunity, Mucosal; Interferon-gamma; Interleukin-4; Macrophages; Male; Mice; Mice, Inbred C57BL; Ovalbumin; Phagocytosis