Journal
FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.758767
Keywords
sex differences; inflammation; bone marrow macrophages; macrophage phenotype; activated fibroblasts
Categories
Funding
- DZHK (German Centre for Cardiovascular Research)
- BMBF (German Ministry of Education and Research)
- German Research Foundation (DFG)
- Charite - Universitatsmedizin Berlin
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The study found that in an inflammatory environment, male mice exhibited stronger polarization and activation of macrophages and cardiac fibroblasts compared to females, suggesting a significant role of sex in cardiac pathologies.
Mounting evidence argues for the significant impact of sex in numerous cardiac pathologies, including myocarditis. Macrophage polarization and activation of cardiac fibroblasts play a key role in myocardial inflammation and remodeling. However, the role of sex in these processes is still poorly understood. In this study, we investigated sex-specific alterations in the polarization of murine bone marrow-derived macrophages (BMMs) and the polarization-related changes in fibroblast activation. Cultured male and female murine BMMs from C57/BL6J mice were polarized into M1 (LPS) and M2 (IL-4/IL-13) macrophages. Furthermore, male and female cardiac fibroblasts from C57/BL6J mice were activated with TNF-alpha, TGF-beta, or conditioned medium from M1 BMMs. We found a significant overexpression of M1 markers (c-fos, NF kappa B, TNF-alpha, and IL-1 beta) and M2 markers (MCP-1 and YM1) in male but not female activated macrophages. In addition, the ROS levels were higher in M1 male BMMs, indicating a stronger polarization. Similarly, the pro-fibrotic markers TGF-beta and IL-1 beta were expressed in activated cardiac male fibroblasts at a significantly higher level than in female fibroblasts. In conclusion, the present study provides strong evidence for the male-specific polarization of BMMs and activation of cardiac fibroblasts in an inflammatory environment. The data show an increased inflammatory response and tissue remodeling in male mice.
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