Interleukin-15 Production at the Early Stage After Oral Infection with Listeria Monocytogenes in Mice

Overview

Journal Immunology

Specialty Allergy & Immunology

Date 1999 Aug 14

PMID 10447719

Citations 9

Authors

A Mitani

H Nishimura

K Hirose

J Washizu

Y Kimura

S Tanaka

G Yamamoto

T Noguchi

Y Yoshikai

Affiliations

Soon will be listed here.

Abstract

We previously reported that exogenous interleukin-15 (IL-15) induces proliferation and activation of intestinal intraepithelial lymphocytes (i-IEL) in naive mice. To investigate the ability of endogenous IL-15 to stimulate i-IEL in vivo, we monitored i-IEL and intestinal epithelial cells (i-EC) in mice after an oral infection with Listeria monocytogenes. Although the populations of alphabeta and gammadelta i-IEL were not significantly changed after the oral infection, the expression level of interferon-gamma (IFN-gamma) was increased both at transcriptional and protein levels, and a conversely marked decrease in interleukin-4 (IL-4) was detected in the i-IEL on day 1 after infection as compared with before infection. The T helper 1 (Th1)-biased response of i-IEL coincided with a peak response of IL-15 production in the i-EC after oral infection. These results suggested that IL-15 produced from i-EC may be at least partly involved in the stimulation of i-IEL to produce IFN-gamma after oral infection with L. monocytogenes.

Citing Articles

Soluble interleukin-15 complexes are generated in vivo by type I interferon dependent and independent pathways.

Anthony S, Howard M, Hailemichael Y, Overwijk W, Schluns K PLoS One. 2015; 10(3):e0120274.

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CXCR3 expression defines a novel subset of innate CD8+ T cells that enhance immunity against bacterial infection and cancer upon stimulation with IL-15.

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Effect of IL-15 and natural killer cells on osteoclasts and osteoblasts in a mouse coculture.

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Irradiation with a low-level diode laser induces the developmental endothelial locus-1 gene and reduces proinflammatory cytokines in epithelial cells.

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Early gene response of human brain microvascular endothelial cells to Listeria monocytogenes infection.

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