HO1 inhibits ROS production and inflammatory response following RSV infection
10.13431/j.cnki.immunol.j.20240031
- VernacularTitle:HO1抑制RSV感染后ROS产生及炎症反应
- Author:
Zhenghong JIANG
1
;
Siyi CHE
;
Enmei LIU
;
Jun XIE
Author Information
1. 400014,重庆医科大学附属儿童医院呼吸中心 国家儿童健康与疾病临床医学研究中心 儿童发育疾病研究教育部重点实验室 儿科学重庆市重点实验室
- Keywords:
Respiratory syncytial virus;
HO1;
ROS;
Inflammation
- From:
Immunological Journal
2024;40(3):242-249
- CountryChina
- Language:Chinese
-
Abstract:
This study aims to investigate the role and specific mechanisms of HO1 in mitigating lung inflammation after RSV infection.An RSV-infected mouse model was established,and lung tissues were collected for RNA-seq and differential gene expression analysis.HE staining and BALF cell counting were used to observe inflammation in the mouse lung tissues.Changes in HO1 expression were detected through immunohistochemistry,Western blotting,and qRT-PCR;inflammatory cytokine levels were assessed using qRT-PCR.HEMIN target proteins were predicted and analyzed by underwent GO and KEGG enrichment test;ROS levels in alveolar epithelial cells were measured using flow cytometry and immunofluorescence.Lysosomal changes were observed using transmission electron microscopy.The results demonstrated that HO1 expression was upregulated in the lung tissues of RSV-infected mice.Inducing HO1 expression alleviated lung tissue pathology,and lowered inflammatory cytokines IL-6 and TNF-α levels.RSV infection promoted ROS release and accumulation in lung epithelial cells,leading to an increase in autolysosomes.The induction of HO1 expression facilitated ROS clearance and reduced the number of autolysosomes.Therefore,the protective effect of HO 1 against oxidative stress reduces intracellular ROS generation,maintains organelle homeostasis,and reducing inflammatory cytokine IL-6,IL-8 and CXCL-10 levels.
