Kim J M, Kim Y J, Cho Y J
Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, Korea.
Scand J Infect Dis. 2000;32(6):643-9. doi: 10.1080/003655400459568.
B. fragilis induces cytokine expression, which can serve as a host signal leading to inflammatory reaction and abscess formation in the peritoneal cavity. We assessed the hypothesis that enteric bacteria may alter the B. fragilis-induced expression of KC genes in mouse peritoneal tissues (MPT). After C57BL/6 mice were inoculated with abscess-forming mixture containing B. fragilis in the presence or absence of E. coli, RNA was extracted from MPT. Expression of KC mRNA was quantified using reverse-transcription polymerase chain reaction and standard RNA. KC and TNFalpha proteins were measured by enzyme-linked immunosorbent assay. KC mRNA in MPT was upregulated following inoculation of B. fragilis and this was paralleled by increased KC protein secretion. When the mice were co-infected with E. coli and B. fragilis intraperitoneally, there was a synergistic increase in the expression of KC of MPT. Co-infection with L. acidophilus and B. fragilis downregulated KC mRNA expression, but co-infection with E. faecalis and B. fragilis synergistically increased KC expression in the infected MPT. Inhibition of TNFalpha production could downregulate KC expression in mixed infected MPT. These results suggest that enteric bacteria may significantly affect the KC signal produced by the host peritoneal cavity in response to B. fragilis infection.
脆弱拟杆菌可诱导细胞因子表达,该表达可作为一种宿主信号,引发炎症反应并导致腹腔脓肿形成。我们评估了以下假说:肠道细菌可能会改变脆弱拟杆菌诱导的小鼠腹膜组织(MPT)中KC基因的表达。在C57BL/6小鼠接种含有脆弱拟杆菌的脓肿形成混合物(存在或不存在大肠杆菌)后,从MPT中提取RNA。使用逆转录聚合酶链反应和标准RNA对KC mRNA的表达进行定量。通过酶联免疫吸附测定法测量KC和TNFα蛋白。接种脆弱拟杆菌后,MPT中的KC mRNA上调,同时KC蛋白分泌增加。当小鼠腹腔内同时感染大肠杆菌和脆弱拟杆菌时,MPT中KC的表达呈协同增加。嗜酸乳杆菌与脆弱拟杆菌共同感染可下调KC mRNA表达,但粪肠球菌与脆弱拟杆菌共同感染可使感染的MPT中KC表达协同增加。抑制TNFα的产生可下调混合感染的MPT中KC的表达。这些结果表明,肠道细菌可能会显著影响宿主腹腔对脆弱拟杆菌感染产生的KC信号。