Affiliations: Department of Applied Biological Chemistry, Graduate
School of Agricultural and Life Sciences, University of Tokyo, 1-1-1 Yayoi,
Bunkyo-ku, Tokyo, 113-8657, Japan | Department of Immunology, National Institute of
Infectious Diseases | Department of Food Science and Technology, College of
Bioresource Sciences, Nihon University | Department of Veterinary Public Health, Graduate
School of Agricultural and Life Sciences, University of Tokyo, Tokyo,
Japan
Abstract: 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.
Keywords: food allergy, oral administration of antigen, intestinal inflammation antigen-specific T cells, Th2 type CD4[TeX:] ^{+} T cells, probiotics, intestinal flora
Journal: BioFactors, vol. 21, no. 1-4, pp. 159-162, 2004
