1. Interleukin-15 may be responsible for early activation of intestinal intraepithelial lymphocytes after oral infection with Listeria monocytogenes in rats.
- Author
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Hirose K, Suzuki H, Nishimura H, Mitani A, Washizu J, Matsuguchi T, and Yoshikai Y
- Subjects
- Animals, Antigens, CD isolation & purification, Antigens, Surface isolation & purification, Interferon-gamma biosynthesis, Intestinal Mucosa cytology, Liver microbiology, Lymphocyte Activation, Male, Mouth Diseases immunology, NF-kappa B metabolism, NK Cell Lectin-Like Receptor Subfamily B, Rats, Rats, Inbred F344, Receptors, Antigen, T-Cell, gamma-delta isolation & purification, Spleen microbiology, Up-Regulation, Interleukin-15 biosynthesis, Intestinal Diseases immunology, Intestinal Mucosa immunology, Lectins, C-Type, Listeriosis immunology, T-Lymphocyte Subsets immunology
- Abstract
Exogenous interleukin-15 (IL-15) stimulates intestinal intraepithelial lymphocytes (i-IEL) from mice to proliferate and produce gamma interferon (IFN-gamma) in vitro. To determine whether endogenous IL-15 is involved in activation of i-IEL during intestinal infection, we examined IL-15 synthesis by intestinal epithelial cells (i-EC) after infection with Listeria monocytogenes in rats. In in vitro experiments, invasion of L. monocytogenes into IEC-6 cells, a rat small intestine epithelial cell line, evidently induced IL-15 mRNA expression coincident with nuclear factor kappaB (NF-kappaB) activation, which is essential for IL-15 gene expression. IL-15 synthesis was detected in rat i-EC on day 1 after an oral inoculation of L. monocytogenes in vivo. The numbers of T-cell receptor (TCR) gamma delta+ T cells, NKR.P1(+) cells, and CD3(+) CD8(+) alpha alpha cells in i-IEL were significantly increased on day 1 after oral infection. The i-IEL from infected rats produced larger amounts of IFN-gamma upon stimulation with immobilized anti-TCR gamma delta or anti-NKR.P1 monoclonal antibodies. These results suggest that IL-15 produced by i-EC may stimulate significant fractions of i-IEL to produce IFN-gamma at an early phase of oral infection with L. monocytogenes.
- Published
- 1998
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