To investigate the mechanisms inducing food-sensitive intestinal inflammation, we focused on the OVA23-3 mouse, a transgenic mouse strain expressing a T cell receptor that recognizes ovalbumin (OVA). Mice administered an egg-white (EW) diet containing OVA showed a trend of loose feces and significant weight loss. Histology of the jejunum showed severe inflammation with villous atrophy. Thus, we studied the role of T cells and intestinal microflora in the development of the inflammation. Severe villous disruption was observed in sections of the jejunum from OVA23-3 mice and RAG-2 gene-deficient OVA23-3 mice fed with EW-diet. Further, a larger number of T cells was found in the lamina propria of the jejunum of EW-diet fed OVA23-3 mice, RAG-2 gene-deficient mice and germfree OVA23-3 mice compared with those of control-diet fed mice. However, severe inflammation was not detected in the jejunum of germfree OVA23-3 mice. CD4+ T cells from the MLN of EW-diet fed OVA23-3 mice showed a Th2 cytokine secretion profile. These observations have thus clarified that antigen-specific Th2 cells play important roles in the development of intestinal inflammation. Although the presence of indigenous bacteria was not essential for the inflammation, T cells could mediate a more severe inflammatory response in their presence.
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