IL-6 enhances the phagocytic function of mouse alveolar macrophages by activating the JAK2/STAT3 signaling pathway.
- Author:
Mengqing HUA
1
;
Peiyu GAO
2
;
Fang FANG
1
;
Haoyu SU
2
;
Chuanwang SONG
3
Author Information
1. Department of Immunology, School of Laboratory Medicine, Bengbu Medical College, Anhui Province Key Laboratory of Immunology in Chronic Diseases, Bengbu 233030, China.
2. Anhui Province Key Laboratory of Immunology in Chronic Diseases, Bengbu 233030, China.
3. Department of Immunology, School of Laboratory Medicine, Bengbu Medical College, Anhui Province Key Laboratory of Immunology in Chronic Diseases, Bengbu 233030, China. *Corresponding author, E-mail: bbmcscw@foxmail.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Mice;
Actins;
Disease Models, Animal;
Interleukin-6;
Janus Kinase 2;
Lipopolysaccharides;
Macrophages, Alveolar;
Signal Transduction
- From:
Chinese Journal of Cellular and Molecular Immunology
2024;40(1):13-18
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of interleukin-6 (IL-6) on the phagocytosis of MH-S alveolar macrophages and its related mechanisms. Methods A mouse acute lung injury (ALI) model was constructed by instilling lipopolysaccharide (LPS) into the airway. ELISA was used to detect the content of IL-6 in bronchoalveolar lavage fluid (BALF). In vitro cultured MH-S cells, in the presence or absence of signal transducer and activator 3 of transcription(STAT3) inhibitor Stattic (5 μmol/L), IL-6 (10 ng/mL~500 ng/mL) was added to stimulate for 6 hours, and then incubated with fluorescent microspheres for 2 hours. The phagocytosis of MH-S cells was detected by flow cytometry. Western blot analysis was used to detect the expression levels of phosphorylated Janus kinase 2 (p-JAK2), phosphorylated STAT3 (p-STAT3), actin-related protein 2 (Arp2) and filamentous actin (F-actin). Results The content of IL-6 in BALF was significantly increased after the mice were injected with LPS through the airway. With the increase of IL-6 stimulation concentration, the phagocytic function of MH-S cells was enhanced, and the expression levels of Arp2 and F-actin proteins in MH-S cells were increased. The expression levels of p-JAK2 and p-STAT3 proteins increased in MH-S cells stimulated with IL-6(100 ng/mL). After blocking STAT3 signaling, the effect of IL-6 in promoting phagocytosis of MH-S cells disappeared completely, and the increased expression of Arp2 and F-actin proteins in MH-S cells induced by IL-6 was also inhibited. Conclusion IL-6 promotes the expression of Arp2 and F-actin proteins by activating the JAK2/STAT3 signaling pathway, thereby enhancing the phagocytic function of MH-S cells.
