Authors
Hongqing Ding, Yi Zhou, Ling Zhao, Mengyi Yuan, Lexuan Wen, Hong Dong, Bingying Liu, Weitao Dong, Hongwei Duan, Xiangguo Wang, Longfei Xiao
Published in
Immunology letters. Pages 107249. Oct 29, 2026. Epub Oct 29, 2026.
Abstract
Mastitis, an inflammation of cow's udder, disrupts the blood-milk barrier (BMB), allowing pathogens to enter the udder and markedly lowering milk yield and quality. Macrophages as immune sentinels in the mammary glands can switch to the M1 pro-inflammatory phenotype thereby exacerbating mastitic damage. However, it remains unclear whether M1 macrophages disrupt the BMB and which mechanisms are involved. Thus, this study quantified BMB disruption and M1 macrophage polarization in bovine mastitic mammary tissue and established a bovine mammary epithelial cell (BMEC)/macrophage co-culture model. Compared with healthy mammary tissue, subclinical and clinical mastitic tissues exhibited a marked reduction in the tight junction (TJ)-related proteins Claudin-1, Occludin, and ZO-1, as well as elevated expression of the M1 markers CD86 and iNOS, and these changes were aggravated with progression from subclinical to clinical mastitis. In vivo, lipopolysaccharide (LPS)-induced M1 macrophages impaired BMEC TJ function, whereas M0 or interleukin-4 (IL-4)-induced M2 macrophages had no effect. In addition, quercetin (Que) restored TJ integrity by inhibiting M1 polarization, an effect that can be attributed to the suppression of NFκB and STAT1 activation. Furthermore, a mouse mastitis model confirmed that Que preserved BMB integrity and reduced M1 infiltration. Collectively, these findings indicate that M1 polarization compromises the BMB and Que protects the BMB by blocking the NFκB and STAT1 signaling pathway.
PMID:
42957054
Bibliographic data and abstract were imported from PubMed on 30 Oct 2026.
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