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B族链球菌对巨噬细胞样细胞系中补体成分C3合成的刺激作用。

Stimulation of complement component C3 synthesis in macrophagelike cell lines by group B streptococci.

作者信息

Goodrum K J

出版信息

Infect Immun. 1987 May;55(5):1101-5. doi: 10.1128/iai.55.5.1101-1105.1987.

Abstract

Complement levels and complement activation are key determinants in streptococcus-induced inflammatory responses. Activation of macrophage functions, such as complement synthesis, by group B streptococci (GBS) was examined as a possible component of GBS-induced chronic inflammation. Using an enzyme-linked immunosorbent assay, secreted C3 from mouse macrophagelike cell lines (PU5-1.8 and J774A.1) was monitored after cultivation with GBS. Whole, heat-killed GBS (1 to 10 CFU per macrophage) of both type Ia and III strains induced 25 to 300% increases in secreted C3 in both cell lines after a 24-h cultivation. GBS-treated cell lines exhibited increases in secreted lysozyme (10%) and in cellular protein (25 to 50%). Inhibition of macrophage phagocytosis by cytochalasin B inhibited GBS stimulation of C3. Purified cell walls of GBS type III strain 603-79 (1 to 10 micrograms/ml) also enhanced C3 synthesis. Local enhancement of macrophage C3 production by ingested streptococci or by persistent cell wall antigens may serve to promote chronic inflammatory responses.

摘要

补体水平和补体激活是链球菌诱导的炎症反应的关键决定因素。B族链球菌(GBS)对巨噬细胞功能(如补体合成)的激活被作为GBS诱导的慢性炎症的一个可能组成部分进行了研究。使用酶联免疫吸附测定法,在用GBS培养后监测从小鼠巨噬细胞样细胞系(PU5-1.8和J774A.1)分泌的C3。Ia型和III型菌株的完整热灭活GBS(每巨噬细胞1至10 CFU)在24小时培养后,在两种细胞系中均诱导分泌的C3增加25%至300%。经GBS处理的细胞系分泌的溶菌酶增加(10%),细胞蛋白增加(25%至50%)。细胞松弛素B对巨噬细胞吞噬作用的抑制抑制了GBS对C3的刺激。III型GBS菌株603-79的纯化细胞壁(1至10微克/毫升)也增强了C3合成。摄入的链球菌或持续存在的细胞壁抗原对巨噬细胞C3产生的局部增强可能有助于促进慢性炎症反应。

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Influence of serotype of group B streptococci on C3 degradation.B族链球菌血清型对C3降解的影响。
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本文引用的文献

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Production of C3 as a marker of lymphokine-mediated macrophage activation.
Cell Immunol. 1984 Aug;87(1):1-14. doi: 10.1016/0008-8749(84)90125-4.

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