Dalal E, Medalia O, Harari O, Aronson M
Department of Cell Biology and Histology, Sackler School of Medicine, Tel Aviv University, Ramat Aviv, Israel.
Infect Immun. 1994 Dec;62(12):5505-10. doi: 10.1128/iai.62.12.5505-5510.1994.
We have previously shown (M. Aronson, O. Medalia, D. Amichay, and O. Nativ, Infect. Immun. 56:1615-1617, 1988) that shedding of viable uroepithelial cells (elicited by invading microorganisms) constitutes an antimicrobial defense mechanism. The present study deals with two different stress-involving procedures, in which increased uroepithelial shedding rendered female mice resistant to vesical infection. Moderate stress was induced in female mice by exposing the animals either to constant illumination for 96 h or to 37 degrees C heat for 24 h. In both cases, the rate of infection was considerably reduced as a result of increased epithelial shedding (P < 0.0001). Stress was manifested by both reduced thymic weight and increased blood corticosterone levels. Shedding was also elicited by intraperitoneal injection of norepinephrine together with hydrocortisone or by intravesical injection of corticosterone. Constant illumination as well as heat enormously facilitated the migration of polymorphonuclear cells into the bladder following the action of chemotactic stimuli. Male mice subjected to identical stress-generating conditions did not display considerable epithelial shedding or increased migration of polymorphonuclear cells, and they were not protected from intravesical infection.
我们之前已经证明(M. 阿隆森、O. 梅达利亚、D. 阿米查伊和O. 纳蒂夫,《感染与免疫》56:1615 - 1617,1988年),(由入侵微生物引发的)活尿路上皮细胞脱落构成一种抗菌防御机制。本研究涉及两种不同的涉及应激的程序,其中尿路上皮脱落增加使雌性小鼠对膀胱感染具有抗性。通过将动物暴露于96小时的持续光照或37摄氏度的热环境24小时,对雌性小鼠诱导适度应激。在这两种情况下,由于上皮脱落增加,感染率显著降低(P < 0.0001)。应激表现为胸腺重量减轻和血液皮质酮水平升高。通过腹腔注射去甲肾上腺素与氢化可的松或膀胱内注射皮质酮也可引发脱落。在趋化刺激作用后,持续光照以及热极大地促进了多形核细胞向膀胱的迁移。处于相同应激产生条件下的雄性小鼠未表现出显著的上皮脱落或多形核细胞迁移增加,并且它们未受到膀胱内感染的保护。