ArticlePloS one2013
Lipopolysaccharide disrupts the milk-blood barrier by modulating claudins in mammary alveolar tight junctions.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 108 citations in OpenAlex.
- Fisetin alleviates lipopolysaccharide-induced mastitis by inhibiting ferroptosis and modulating the gut microbiota.The veterinary quarterly · 2026Article
- Prevalence, Virulence, and Pathogenic Mechanisms of Mastitis-AssociatedVeterinary sciences · 2026Review
- Dynamics of the milk microbial community during subacute ruminal acidosis with or without intramammary lipopolysaccharide challenge in dairy cows.Animal microbiome · 2026Article
- A novel, cost-effective approach to cell-cultured milk production: Progesterone and MMP inhibition promote lactogenic differentiation in bovine mammary epithelial cells.Food chemistry: X · 2026Article
- Article
- Mammary Epithelial Cell Spheroid: Stabilization Through Vascular-Wall Mesenchymal Stem Cells and Endothelial Cells Co-Culture.Animals : an open access journal from MDPI · 2025Article
- Claudin Proteins: Their Potential Role in Obesity and Adipose Tissue Signaling, Physiology and Disease.Nutrients · 2025Review
- Targeted Regulation of HSP70 by the ARP2/3 Complex in Mammary Epithelial Cells and Its Impact on Host Cell Apoptosis.Biomolecules · 2025Article
- Deciphering the colostral-immunity transfer: from mammary gland to neonates small intestine.Veterinary research communications · 2025Review
- Investigating the role of the mPGES-PGE₂-EP4 pathway inFrontiers in veterinary science · 2025Article
- Effects of topical application of resveratrol on tight junction barrier and antimicrobial compound production in lactating goat mammary glands.Veterinary research · 2024Article
- Breast milk concentrations of acetaminophen and diclofenac - unexpectedly high mammary transfer of the general-purpose drug acetaminophen.BMC pregnancy and childbirth · 2024Article
- Potential effects of gingerol topical application on components of the innate immunity in lactating goat mammary glands.Innate immunity · 2023Article
- Severity of Clinical Mastitis and Bacterial Shedding.Pathogens (Basel, Switzerland) · 2023Article
- Bacteremia in Severe Mastitis of Dairy Cows.Microorganisms · 2023Article
- iE-DAP Induced Inflammatory Response and Tight Junction Disruption in Bovine Mammary Epithelial Cells via NOD1-Dependent NF-κB and MLCK Signaling Pathway.International journal of molecular sciences · 2023Article
- Valine Treatment Enhances Antimicrobial Component Production in Mammary Epithelial Cells and the Milk of Lactating Goats Without Influencing the Tight Junction Barrier.Journal of mammary gland biology and neoplasia · 2023Article
- Short Chain Fatty Acids (SCFAs) Are the Potential Immunomodulatory Metabolites in ControllingNutrients · 2022Review
- The Rumen Microbiota Contributes to the Development of Mastitis in Dairy Cows.Microbiology spectrum · 2022Article
- Investigating mammary glands of lactating goats for the presence of tertiary lymphoid organs.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mastitis, inflammation of the mammary gland, is the most costly common disease in the dairy industry, and is caused by mammary pathogenic bacteria, including Escherichia coli. The bacteria invade the mammary alveolar lumen and disrupt the blood-milk barrier. In normal mammary gland, alveolar epithelial tight junctions (TJs) contribute the blood-milk barrier of alveolar epithelium by blocking the leakage of milk components from the luminal side into the blood serum. In this study, we focused on claudin subtypes that participate in the alveolar epithelial TJs, because the composition of claudins is an important factor that affects TJ permeability. In normal mouse lactating mammary glands, alveolar TJs consist of claudin-3 without claudin-1, -4, and -7. In lipopolysaccharide (LPS)-induced mastitis, alveolar TJs showed 2-staged compositional changes in claudins. First, a qualitative change in claudin-3, presumably caused by phosphorylation and participation of claudin-7 in alveolar TJs, was recognized in parallel with the leakage of fluorescein isothiocyanate-conjugated albumin (FITC-albumin) via the alveolar epithelium. Second, claudin-4 participated in alveolar TJs with claudin-3 and claudin-7 12 h after LPS injection. The partial localization of claudin-1 was also observed by immunostaining. Coinciding with the second change of alveolar TJs, the severe disruption of the blood-milk barrier was recognized by ectopic localization of β-casein and much leakage of FITC-albumin. Furthermore, the localization of toll-like receptor 4 (TLR4) on the luminal side and NFκB activation by LPS was observed in the alveolar epithelial cells. We suggest that the weakening and disruption of the blood-milk barrier are caused by compositional changes of claudins in alveolar epithelial TJs through LPS/TLR4 signaling.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.