ArticleJournal of animal science and biotechnology2025
β-Hydroxybutyrate-induced mitochondrial DNA (mtDNA) release mediated innate inflammatory response in bovine mammary epithelial cells by inhibiting autophagy.
Article in Journal of animal science and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Emerging host-directed strategies for overcoming drug resistance and immune evasion in Staphylococcus aureus infections.Journal of advanced research · 2026Review
- Mitochondrial DNA as a driver of inflammation via the cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Mitochondrial dysfunction in the bovine mammary gland: regulatory mechanisms and therapeutic strategies.Journal of animal science and biotechnology · 2026Review
- Knockout of theVeterinary sciences · 2026Article
- Microbiota-derived indole-3-acetic acid alleviates rumen epithelial barrier dysfunction during the peripartum period through AhR signaling.NPJ biofilms and microbiomes · 2025Article
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9 authors.
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Abstract
backgroundIn perinatal dairy cows, ketosis is a prevalent metabolic disorder that lowers milk output and performance. Mitochondrial dysfunction and chronic inflammation in mammary tissue are linked to elevated blood ketone levels, particularly β-hydroxybutyrate (BHB). Recent research has linked cytosolic mitochondrial DNA (mtDNA) with chronic aseptic inflammation by activating the cGAS-STING pathway during metabolic disorders, while autophagy activation effectively reverses this process. However, whether it is involved in mammary gland damage during ketosis is poorly understood. Therefore, this study aimed to explore the underlying mechanisms of mtDNA-induced inflammation under BHB stress and evaluate the potential therapeutic strategy of autophagy activation in mitigating this damage.
resultsOur study found an increased cytoplasmic mtDNA abundance in mammary gland tissues of dairy cows with ketosis and bovine mammary epithelial cell line (MAC-T) subjected to BHB stress. Further investigations revealed the activation of the cGAS-STING pathway and inflammatory response, indicated by elevated levels of cGAS and STING, along with increased phosphorylation levels of TBK1, P65, and IκB, and higher transcript levels of pro-inflammatory factors (IL-1B, IL-6, and TNF-α) in both in vivo and in vitro experiments. Notably, STING inhibition via si-STING transfection reversed BHB-induced inflammation. Additionally, autophagy activation appeared to protect against BHB stress by facilitating the removal of cytoplasmic mtDNA and preventing cGAS-STING pathway-mediated inflammation.
conclusionsThe findings illustrate that elevated BHB levels lead to the release of cytoplasmic mtDNA, which in turn activates the cGAS-STING pathway and triggers an inflammatory response in the mammary glands during hyperketonemia. Conversely, autophagy activation has been shown to alleviate this process by promoting cytoplasmic mtDNA degradation.
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