ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
HCAR2 Modulates the Crosstalk between Mammary Epithelial Cells and Macrophages to Mitigate Staphylococcus aureus Infection in the Mouse Mammary Gland.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Echinatin attenuates LPS-induced mastitis by suppressing IL-17RA and MAPK/NF-κB signaling.BMC veterinary research · 2026Article
- Emerging host-directed strategies for overcoming drug resistance and immune evasion in Staphylococcus aureus infections.Journal of advanced research · 2026Review
- The NLRP3-CASP1 Axis Contributes to Pyroptosis in Bovine Mammary Epithelial Cells During Clinical Mastitis.Antioxidants (Basel, Switzerland) · 2026Article
- The dialogue between breast cancer and microorganisms.Frontiers in cellular and infection microbiology · 2026Review
- Overexpression of mitofusin 2 ameliorates inflammation and oxidative stress in lipopolysaccharide-induced mastitis model by regulating phosphofurin acidic cluster sorting protein 2.Animal models and experimental medicine · 2026Article
- Lactoferrin-cyanidin-3-glucoside nanoparticles alleviate inflammation and oxidative stress viaMaterials today. Bio · 2025Article
- Anthocyanins Prevent Mastitis Exacerbation by Inhibiting PANoptosis Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- HCAR2 Modulates the Crosstalk between Mammary Epithelial Cells and Macrophages to Mitigate Staphylococcus aureus Infection in the Mouse Mammary Gland.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Staphylococcus aureus (S. aureus) is a major zoonotic pathogen, with mammary gland infections contributing to mastitis, a condition that poses significant health risks to lactating women and adversely affects the dairy industry. Therefore, understanding the immune mechanisms underlying mammary infections caused by S. aureus is essential for developing targeted therapeutic strategies against mastitis. This study identified hydroxycarboxylic acid receptor 2 (HCAR2) as a potential regulator of S. aureus infection in mammary glands. It is demonstrated that HCAR2 deficiency exacerbates the inflammatory response and disrupts the blood-milk barrier in the mammary gland during S. aureus infection, with NLRP3 inflammasome-mediated pyroptosis playing a central role. Activation of HCAR2, on the other hand, suppressed CMPK2 expression, thereby mitigating mitochondrial damage and pyroptosis in mouse mammary epithelial cells (mMECs) induced by S. aureus. Additionally, mitochondrial DNA (mtDNA) released from S. aureus-infected mMECs activates the cGAS/STING signaling pathway in macrophages, impairing their bactericidal activity. In conclusion, this study highlights the critical role of HCAR2 in S. aureus infection of the mammary gland and provides a theoretical basis for identifying potential therapeutic targets for such infections.
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