Müller-Alouf H, Alouf J E, Gerlach D, Ozegowski J H, Fitting C, Cavaillon J M
Unité des Toxines Microbiennes, URA 557 Centre National de la Recherche Scientifique, Paris, France.
Infect Immun. 1994 Nov;62(11):4915-21. doi: 10.1128/iai.62.11.4915-4921.1994.
The differences between toxic or septic shocks in humans during infections by streptococci and gram-negative bacteria remain to be fully characterized. For this purpose, a quantitative study of the cytokine-inducing capacity of Streptococcus pyogenes erythrogenic (pyrogenic) exotoxins (ETs) A and C, heat-killed S. pyogenes bacteria, and Neisseria meningitidis endotoxin (lipopolysaccharide [LPS]) on human peripheral blood mononuclear cells (PBMC) and monocytes has been undertaken. The levels of interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-6, IL-8, tumor necrosis factor alpha (TNF-alpha), and TNF-beta induced by these bacterial products and bacteria were determined by using cell supernatants. The capacity of ETs to elicit the monocyte-derived cytokines IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha was found to depend on the presence of T lymphocytes, because of the failure of purified monocytes to produce significant amounts of these cytokines in response to ETs. PMBC elicited large amounts of these cytokines, as well as IL-8 and TNF-beta, with an optimal release after 48 to 96 h. The most abundant cytokine produced in response to ETA was IL-8. In contrast to the superantigens ETA and ETC, LPS and heat-killed streptococci stimulated the production of significant amounts of IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha, with optimal production after 24 to 48 h in monocytes, indicating no significant involvement of T cells in the process. ETs, but neither LPS nor streptococci, were potent inducers of TNF-beta in PBMC. This study outlines the differences in the pathophysiological features of shock evoked by endotoxins and superantigens during infection by gram-negative bacteria and group A streptococci, respectively. The production of TNF-alpha was a common pathway for LPS, streptococcal cells, and ETs, although cell requirements and kinetics of cytokine release were different.
人类在感染链球菌和革兰氏阴性菌期间,中毒性休克或脓毒性休克之间的差异仍有待全面阐明。为此,已对化脓性链球菌致热外毒素(ETs)A和C、热灭活的化脓性链球菌以及脑膜炎奈瑟菌内毒素(脂多糖[LPS])对人外周血单核细胞(PBMC)和单核细胞的细胞因子诱导能力进行了定量研究。通过使用细胞上清液来测定这些细菌产物和细菌诱导的白细胞介素-1α(IL-1α)、IL-1β、IL-6、IL-8、肿瘤坏死因子α(TNF-α)和TNF-β的水平。发现ETs引发单核细胞衍生细胞因子IL-1α、IL-1β、IL-6和TNF-α的能力取决于T淋巴细胞的存在,因为纯化的单核细胞在对ETs作出反应时未能产生大量这些细胞因子。PBMC能引发大量这些细胞因子以及IL-8和TNF-β,在48至96小时后达到最佳释放量。对ETA反应产生的最丰富细胞因子是IL-8。与超抗原ETA和ETC不同,LPS和热灭活的链球菌刺激产生大量的IL-1α、IL-1β、IL-6和TNF-α,单核细胞在24至48小时后产生量最佳,表明T细胞在此过程中无显著参与。ETs,但LPS和链球菌均不是PBMC中TNF-β的有效诱导剂。本研究概述了革兰氏阴性菌和A组链球菌感染期间内毒素和超抗原诱发休克在病理生理特征上的差异。TNF-α的产生是LPS、链球菌细胞和ETs的共同途径,尽管细胞需求和细胞因子释放动力学有所不同。