Induction of the chemokine beta peptides, MIP-1 alpha and MIP-1 beta, by lipopolysaccharide is differentially regulated by immunomodulatory cytokines gamma-IFN, IL-10, IL-4, and TGF-beta.

摘要: The macrophage occupies a central role in the host response to invasion, exerting its control over developing inflammatory largely through elaboration of an assortment endogenous mediators including many cytokines. beta chemokine peptides, protein [MIP]-1 alpha and MIP-1 beta, are two such effectors markedly up-regulated macrophages following exposure bacterial lipopolysaccharide (LPS). These highly homologous like other members family, exhibit diverse but partially overlapping biological activity profiles, suggesting that cellular participants intensity may part be regulated by selective expression these chemokines. Studies reported here demonstrate that, contrast "balanced" alpha/MIP-1 responses LPS-stimulated cultures vitro, circulating levels significantly higher than those LPS administration vivo. Further studies have revealed several immunomodulatory cytokines known vivo as consequence invasive stimulus (gamma-IFN, IL-10, IL-4, transforming growth factor [TGF]-beta) down-regulated LPS-induced release spared response. This altered pattern secretion explain, at least part, high relative observed challenge.