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发霉房屋中的链霉菌孢子诱导 RAW264.7 巨噬细胞系分泌一氧化氮、TNFα 和 IL-6,而不会导致随后的细胞死亡。

Streptomyces spores from mouldy houses induce nitric oxide, TNFα and IL-6 secretion from RAW264.7 macrophage cell line without causing subsequent cell death.

机构信息

Division of Environmental Health, National Public Health Institute, P.O. Box 95, FIN-70701 Kuopio, Finland.

出版信息

Environ Toxicol Pharmacol. 1997 Feb 15;3(1):57-63. doi: 10.1016/s1382-6689(96)00140-8.

Abstract

The current view is that only bacterial lipopolysaccharide (LPS) and gamma interferon (IFNγ) are able to alone activate macrophages to secrete nitric oxide (NO), probably a causative agent of cell death. Moreover, some cytokines and gram positive pathogens together with IFNγ induce NO-production. Surprisingly, spores of Streptomyces sp., which are mesophilic gram-positive bacteria found in mouldy houses, stimulated RAW264.7 macrophages to produce pro-inflammatory cytokines, tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6), and induced the expression of inducible NO-synthase (iNOS) with a subsequent NO-production. However, the Streptomyces spores did not kill NO-producing macrophages, as did both LPS and gram negative bacteria Pseudomonas fluorescens, strong inducers of cytokine- and NO-production. These results imply that Streptomyces sp., induced cytokine and NO-secretion, may play a role in the responses evoked by exposure to these microbes. Moreover, factors other than, or in addition to NO, are necessary for cytotoxicity in murine macrophages.

摘要

目前的观点认为,只有细菌脂多糖(LPS)和γ干扰素(IFNγ)能够单独激活巨噬细胞分泌一氧化氮(NO),NO 可能是细胞死亡的原因之一。此外,一些细胞因子和革兰氏阳性病原体与 IFNγ 一起诱导 NO 的产生。令人惊讶的是,链霉菌属的孢子,一种在发霉的房屋中发现的嗜温性革兰氏阳性细菌,刺激 RAW264.7 巨噬细胞产生促炎细胞因子,肿瘤坏死因子-α(TNFα)和白细胞介素-6(IL-6),并诱导诱导型一氧化氮合酶(iNOS)的表达,随后产生 NO。然而,链霉菌孢子并没有像 LPS 和革兰氏阴性细菌荧光假单胞菌那样杀死产生 NO 的巨噬细胞,荧光假单胞菌是细胞因子和 NO 产生的强诱导剂。这些结果表明,链霉菌属诱导细胞因子和 NO 的分泌,可能在暴露于这些微生物引起的反应中发挥作用。此外,除了 NO 之外,或除了 NO 之外,还有其他因素对于鼠巨噬细胞的细胞毒性是必需的。

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