McHugh S, Yamamoto Y, Klein T W, Friedman H
Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa 33612, USA.
Can J Microbiol. 2000 Oct;46(10):885-91.
Infection of macrophages from genetically susceptible A/J mice with Legionella pneumophila induces high levels of various cytokines in serum as well as in cultures of spleen or peritoneal cells from the mice. However, modulation of receptor expression for these cytokines during infection has not been studied in detail, even though these receptors on macrophages have a critical role in inflammatory responses during the infection. In the present study, the differential expression of mRNA for TNF and IL-1 receptors as well as receptor antigens during infection of macrophages with virulent vs. avirulent L. pneumophila was investigated. Mouse thioglycollate-elicited peritoneal macrophages showed by RT-PCR constitutive steady-state levels of mRNA for TNF-type I and -type II receptors as well as IL-1 type I receptor. However, IL-1 type II receptor mRNA was not expressed in thioglycollate-elicited macrophages. Infection of macrophages with virulent bacteria caused an upregulation of IL-1 type I and TNF type I receptor mRNA, but had no effect on TNF type II receptor message. Avirulent L. pneumophila infection caused much less induction of these receptor mRNAs. The amount of receptor antigen of IL-1 type I on the surface of macrophages was also increased by infection with virulent L. pneumophila determined by flow cytometric analysis. These results indicate that L. pneumophila infection not only causes induction of various cytokines, but also modulation of certain cytokine receptors, which may regulate the susceptibility to infection.
用嗜肺军团菌感染基因易感的A/J小鼠的巨噬细胞，会在血清以及小鼠脾脏或腹膜细胞培养物中诱导产生高水平的多种细胞因子。然而，尽管巨噬细胞上的这些受体在感染期间的炎症反应中起关键作用，但在感染期间这些细胞因子受体表达的调节尚未得到详细研究。在本研究中，研究了用有毒力与无毒力的嗜肺军团菌感染巨噬细胞期间，TNF和IL-1受体的mRNA以及受体抗原的差异表达。通过RT-PCR检测发现，小鼠巯基乙酸盐诱导的腹膜巨噬细胞中，TNF I型和II型受体以及IL-1 I型受体的mRNA呈组成型稳态水平。然而，IL-1 II型受体mRNA在巯基乙酸盐诱导的巨噬细胞中未表达。用有毒力的细菌感染巨噬细胞会导致IL-1 I型和TNF I型受体mRNA上调，但对TNF II型受体的信息没有影响。无毒力的嗜肺军团菌感染对这些受体mRNA的诱导作用要小得多。通过流式细胞术分析确定，用有毒力的嗜肺军团菌感染也会增加巨噬细胞表面IL-1 I型受体抗原的量。这些结果表明，嗜肺军团菌感染不仅会诱导多种细胞因子产生，还会调节某些细胞因子受体，这可能会调节对感染的易感性。
