期刊
INFECTION AND IMMUNITY
卷 76, 期 8, 页码 3651-3656出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.00358-08
关键词
-
资金
- National Institutes of Health [DK38327,, DK058755,, P30 DK034928]
Substance P is a tachykinin that enhances pathways of inflammation. Leukocytes at sites of intestinal inflammation make substance P. This study explored the role of interieukin-12 (IL42), IL-23, and the regulatory cytokines IL-10 and transforming growth factor P (TGF-beta) in controlling leukocyte substance P production. In murine schistosomiasis, it was found that IL-12 and IL-23 drive substance P gene expression and peptide synthesis in murine splenic T cells and macrophages, respectively. Cytokine induction of substance P synthesis both in T cells and in macrophages depends on intracellular NF-kappa B activation and is Stat4 independent. IL-10 inhibits T-cell substance P production, while TGF-beta blocks macrophage substance P expression. Intestinal macrophages also produce substance P, subject mostly to IL-23 and TGF-beta regulation. Hemokinin is another tachykinin with homology to substance P. Macrophages and T cells make hemokinin, but hemokinin production is not subject to IL-12 or IL-23 regulation.
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