Garzelli C, Campa M, Colizzi V, Benedettini G, Falcone G
Infect Immun. 1982 Jan;35(1):13-9. doi: 10.1128/iai.35.1.13-19.1982.
Experimental infection of mice with Pseudomonas aeruginosa resulted in the polyclonal activation of B lymphocytes, as assessed by the spontaneous plaque-forming cell (PFC) response to trinitrophenyl and sheep erythrocytes. Additionally, a PFC response to bromelain-treated syngeneic erythrocytes (Br-MRBC) could be detected in infected mice, suggesting that P. aeruginosa infection might also induce activation of self-reactive B-cell clones and consequently lead to autoantibody production. Furthermore, in cultures of mouse peritoneal cells, heat-killed P. aeruginosa enhanced the development of anti-Br-MRBC PFC, even under conditions where cell division was blocked, suggesting that the in vitro P. aeruginosa-induced enhancement of anti-Br-MRBC PFC was essentially related to cell differentiation, cell division playing only a minor role. The mechanism of the in vivo and in vitro P. aeruginosa-induced activation of anti-Br-MRBC PFC are discussed.
用铜绿假单胞菌对小鼠进行实验性感染,通过对三硝基苯和绵羊红细胞的自发空斑形成细胞(PFC)反应评估,结果显示B淋巴细胞出现多克隆激活。此外,在感染小鼠中可检测到对菠萝蛋白酶处理的同基因红细胞(Br-MRBC)的PFC反应,这表明铜绿假单胞菌感染可能还会诱导自身反应性B细胞克隆的激活,从而导致自身抗体产生。此外,在小鼠腹膜细胞培养物中,热灭活的铜绿假单胞菌即使在细胞分裂受阻的条件下也能增强抗Br-MRBC PFC的发育,这表明体外铜绿假单胞菌诱导的抗Br-MRBC PFC增强主要与细胞分化有关,细胞分裂仅起次要作用。本文讨论了体内和体外铜绿假单胞菌诱导抗Br-MRBC PFC激活的机制。