Candida albicans-induced acute lung injury through activating several inflammatory signaling pathways in mice.

Authors:
Lin Fu
Lin Fu
Taichung Veterans General Hospital
Taiwan
Ling Zheng
Ling Zheng
University of Southern California
United States
Jing Ye
Jing Ye
Fourth Military Medical University
China
Jia-Bin Li
Jia-Bin Li
The First Affiliated Hospital of Anhui Medical University
China

Int Immunopharmacol 2019 Apr 17;72:275-283. Epub 2019 Apr 17.

Department of Infectious Diseases, The First Affiliated Hospital, Anhui Medical University, Hefei 230032, China; Anhui Center for Surveillance of Bacterial Resistance, Hefei 230032, China. Electronic address:

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.

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Source
https://linkinghub.elsevier.com/retrieve/pii/S15675769183145
Publisher Site
http://dx.doi.org/10.1016/j.intimp.2019.04.026DOI Listing
April 2019
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