Substance P Diminishes Lipopolysaccharide and Interferon-gamma-Induced TGF-beta1 Production by Cultured Murine Macrophages

Author： Marriott I. Bost K.L.

Publisher： Academic Press

ISSN： 0008-8749

Source： Cellular Immunology, Vol.183, Iss.2, 1998-02, pp. : 113-120

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Abstract

Recent evidence has demonstrated the importance of substance P and its receptor in macrophage-mediated inflammatory responses. While previous studies have shown that substance P can augment proinflammatory monokine production, little is known about the effects of this neuropeptide on the production of monokines that might limit inflammation. In the present study we have investigated the effect of substance P treatment on the production of transforming growth factor-beta1 (TGF-beta1) in cultured murine macrophages. We report that, while substance P agonist alone elicited increases in TGF-beta1 mRNA expression and modest increases in TGF-beta1 secretion, substance P dramatically diminished LPS- or IFN-gamma-induced TGF-beta1 production. These results suggest a previously unrecognized mechanism where substance P may act as a proinflammatory mediator by limiting the production of excessive levels of TGF-beta1 by LPS- or IFN-gamma-activated macrophages. Copyright 1998 Academic Press.