Department of Infectious Diseases, The First Affiliated Hospital, Anhui Medical University, Hefei 230032, China; Second Affiliated Hospital, Anhui Medical University, Hefei 230032, China.
Second Affiliated Hospital, Anhui Medical University, Hefei 230032, China.
Int Immunopharmacol. 2019 Jul;72:275-283. doi: 10.1016/j.intimp.2019.04.026. Epub 2019 Apr 17.
Candida albicans infection-induced acute lung injury is one of the most prevalent diseases in immunosuppressive individual. Nevertheless, the mechanism by which Candida albicans induced acute lung injury remains unclear. The present study investigated the mechanism by which Candida albicans induced acute lung injury in mice. Mice were randomly divided into four groups and intratracheally injected with 60 μl Candida albicans (10 CFU) or normal saline. Half of the mice were sacrificed at 6 h after Candida albicans. The rest of the mice for survival test were observed until 7 d after Candida albicans. As expected, immunosuppression aggravated Candida albicans-induced acute lung injury and death in mice. Additionally, Candida albicans infection elevated mRNA levels of pro-inflammatory and chemokines in lungs and the levels of IL-6, IL-1β and IL-17 in serum. Further study showed that Candida albicans promoted nuclear translocation of NF-κB p50 and p65 subunits in pulmonary epithelial cells and interstitial cells. Candida albicans induced pulmonary p38, ERK1/2 and Akt phosphorylation in normal and immunosuppressive mice. Moreover, Candida albicans infection activated pulmonary STAT3 signaling in normal and immunosuppressive mice. Overall, these results suggest that Candida albicans induced acute lung injury and death may be through activating several inflammatory signaling pathways.
白色念珠菌感染诱导的急性肺损伤是免疫抑制个体中最常见的疾病之一。然而，白色念珠菌诱导急性肺损伤的机制尚不清楚。本研究探讨了白色念珠菌诱导小鼠急性肺损伤的机制。小鼠随机分为四组，经气管内注射 60μl 白色念珠菌（10 CFU）或生理盐水。半数小鼠在白色念珠菌注射后 6 h 处死。其余用于生存试验的小鼠观察至白色念珠菌注射后 7 d。正如预期的那样，免疫抑制加重了白色念珠菌诱导的小鼠急性肺损伤和死亡。此外，白色念珠菌感染增加了肺部促炎细胞因子和趋化因子的 mRNA 水平以及血清中 IL-6、IL-1β 和 IL-17 的水平。进一步的研究表明，白色念珠菌促进了肺上皮细胞和间质细胞中 NF-κB p50 和 p65 亚基的核易位。在正常和免疫抑制小鼠中，白色念珠菌诱导了肺 p38、ERK1/2 和 Akt 的磷酸化。此外，白色念珠菌感染激活了正常和免疫抑制小鼠的肺 STAT3 信号通路。综上所述，这些结果表明，白色念珠菌诱导的急性肺损伤和死亡可能是通过激活几种炎症信号通路。
