Affiliation:
1. Department of public health laboratory sciences, School of public health, Hengyang Medical School, University of South China , Hengyang, China
2. Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University , Changsha, China
3. Institute of Pathogenic Biology, Hengyang Medical School, University of South China , Hengyang, China
Abstract
ABSTRACT
Chlamydia psittaci
is a human pathogen that causes atypical pneumonia after zoonotic transmission. We confirmed that
C. psittaci
infection induces oxidative stress in human bronchial epithelial (HBEs) cells and explored how this is regulated through miR-184 and the Wnt/β-catenin signaling pathway. miR-184 mimic, miR-184 inhibitor, FOXO1 siRNA, or negative control sequence was transfected into HBE cells cultured in serum-free medium using Lipofectamine 2000. Then, prior to the cells were infected with
C. psittaci
6BC, and the cells were treated with or without 30 µM Wnt/β-catenin inhibitor ICG-001. Quantification of reactive oxygen species, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione was carried out according to the manufacturer’s protocol using a corresponding assay kit. The outcome of both protein and gene was measured by western blotting or real-time fluorescence quantitative PCR. In
C. psittaci
-infected HBE cells, miR-184 was upregulated, while one of its target genes,
FOXO1
, was downregulated. ROS and MDA levels increased, while SOD and GSH contents decreased after
C. psittaci
infection. When miR-184 expression was downregulated, the level of oxidative stress caused by
C. psittaci
infection was reduced, and the Wnt/β-catenin signaling pathway was inhibited. The opposite results were seen when miR-184 mimic was used. Transfecting with FOXO1 siRNA reversed the effect of miR-184 inhibitor. Moreover, when the Wnt/β-catenin-specific inhibitor ICG-001 was used, the level of oxidative stress induced by
C. psittaci
infection was significantly suppressed. miR-184 can target FOXO1 to promote oxidative stress in HBE cells following
C. psittaci
infection by activation of the Wnt/β-catenin signaling pathway.
Funder
HSTD | Natural Science Foundation of Hunan Province
Scientific Research Fund of Hunan Provincial Education Department
Graduate Research Innovation Project of Hunan Province
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
2 articles.
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