NLRP3 is involved in interaction between myofibroblasts and M1-type macropha-ges in dairy cows
10.16303/j.cnki.1005-4545.2024.07.21
- VernacularTitle:NLRP3参与奶牛肌成纤维细胞和M1型巨噬细胞的相互作用
- Author:
Yunjie BAI
1
;
Jiamin ZHAO
;
Zhiguo GONG
;
Wenhui BAO
;
Zhuoya YU
;
Chao WANG
;
Wei MAO
;
Shuangyi ZHANG
;
Bo LIU
Author Information
1. 内蒙古农业大学兽医学院,内蒙古呼和浩特 010010
- Keywords:
NLRP3;
myofibroblasts;
macrophages;
dairy cow
- From:
Chinese Journal of Veterinary Science
2024;44(7):1507-1513,1520
- CountryChina
- Language:Chinese
-
Abstract:
During the process of dairy farming,various factors such as physical injury and bacterial infection act upon body tissues or organs,leading to the disruption of skin or mucous tissue integ-rity and subsequent tissue injury and trauma.The healing of these injuries is a complex process that necessitates the coordinated efforts of different cells and involvement of diverse cytokines.A-mong them,the interaction between macrophages and myofibroblasts is indispensable for efficient tissue repair.Nod-like receptor protein 3(NLRP3),a pattern recognition receptor in the innate im-mune system,may play a regulatory role in modulating this intricate process.In this study,cow myofibroblasts and M1 type bone marrow-derived macrophages were cultured in vitro,followed by collection of cell culture supernatant for co-culture analysis.Both cytokine secretion levels in M1 type bone marrow-derived macrophages as well as expression patterns levels of myofibroblast growth factor protein and mRNA were detected.The regulatory mechanism underlying NLRP3 in-volvement in mediating interactions between these two cell types was investigated using NLRP3 inhibitor MCC950.The results showed that an effective method for culturing cow muscle fibroblasts in vitro was successfully established and myofibroblast conditioned medium(MFbCM)could regulate M1 macrophage secretion profiles.Moreover,M1 macrophage conditioned medium(M1?CM)was found to influence myofibroblast growth factor expression levels.Our findings sug-gest that NLRP3 plays a significant regulatory role during crosstalk between myofibroblasts and M1-type pro-inflammatory macrophages.
