Effects of heme oxygenase-1 on autophagy regulation and intracellular growth of Mycobacterium abscessus
10.3969/j.issn.1000-484X.2025.04.017
- VernacularTitle:血红素氧化酶1调控自噬对脓肿分枝杆菌胞内生长的影响
- Author:
Aifeng LIU
1
;
Haijun LUO
1
;
Renfeng XIE
1
;
Xiaohua MA
1
Author Information
1. 长沙市中心医院,长沙 410004
- Publication Type:Journal Article
- Keywords:
Mycobacterium abscessus;
Heme oxygenase-1;
Autophagy;
Colony count
- From:
Chinese Journal of Immunology
2025;41(4):873-878
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the role of heme oxygenase-1(HO-1)regulating autophagy and its impact on the intracel-lular growth of Mycobacterium abscessus(M.abs).Methods:The standard strain of M.abs ATCC19977 was used to stimulate mouse RAW264.7 macrophages with a specified multiple of infection(MOI)for a specified time.Western blot analysis was performed to detect the expression levels of HO-1 protein and autophagy related proteins Atg5,LC3Ⅱ and p62.Macrophages were pretreated with HO-1 specific inducer CoPP and enzyme activity inhibitor SnPP for 12 h,and incubated with M.abs for 2 h.Amikacin removed extra-cellular bacteria and continued to culture until the specified time,and cell activity was detected by CCK-8 method.Western blot and LysoTracker Red were used to detect the regulatory relationship between HO-1 protein and autophagy related proteins.Bacterial survival and TNF-α secretion levels were detected by colony count and ELISA.Results:Compared with the control group,M.abs could induce increased expression of HO-1,Atg5,LC3Ⅱ and p62 proteins.Over-expression and inhibition of HO-1 were found to effectively regu-late the expressions of Atg5,LC3Ⅱ and p62 induced by M.abs.LysoTracker Red,colony count,and ELISA results demonstrated that SnPP promoted the increasement of intracellular lysosomes,significantly inhibited M.abs intracellular proliferation,and reduced TNF-α secretion.Conclusion:Inhibition of HO-1 can enhance the autophagy flow induced by M.abs and reduce the intracellular growth of M.abs,which provides scientific basis for the development of targeted drugs targeting HO-1.
