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Peer-reviewedCC BY-NC 4.0The Veterinary Quarterly

Heat stress enhances Klebsiella pneumoniae-induced cellular injury and impairs milk fat synthesis in bovine mammary epithelial cells

  • Jia Guo1
  • Zhihao Wang1,2
  • Haoran Zhong3
  • Pengfei Dong1
  • Kangjun Liu1
  • Long Guo1
  • Luying Cui1
  • Junsheng Dong1
  • Jianji Li1
  • Guoqiang Zhu1
  • Ran Wang4
  • Lili Zhang4
2 more authors
  • Xia Meng1
  • Heng Wang1
4 affiliations
  1. 1College of Veterinary Medicine, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou, China
  2. 2Pancreatic Center, Department of Gastroenterology, Yangzhou Key Laboratory of Pancreatic Disease, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China
  3. 3Key Laboratory of Animal Schistosomiasis of Ministry of Agriculture and Rural Affairs, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Shanghai, China
  4. 4Institute of Food Safety and Nutrition, Jiangsu Academy of Agricultural Sciences, Nanjing, China
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Abstract

Heat stress (HS) poses a significant threat to dairy production by reducing milk yield and elevating the incidence of mastitis. Concurrently, mastitis caused by Klebsiella pneumoniae (K. pneumoniae) occurs more frequently during the summer months, further exacerbating udder health challenges. Our study demonstrates that combined HS and K. pneumoniae exposure significantly exacerbates cellular damage of bovine mammary epithelial cells (BMECs). Mechanistically, HS potentiates K. pneumoniae-induced NF-κB pathway activation and reactive oxygen species (ROS) accumulation, leading to upregulated pro-inflammatory cytokines, chemokines, and antimicrobial peptides. Simultaneously, HS disrupts tight junction integrity, downregulating ZO-1, Occludin, and Claudins, and compromises the epithelial barrier. Critically, HS further suppresses lipid accumulation and the expression of milk fat synthesis-related genes and proteins in K. pneumoniae-challenged BMECs. This metabolic suppression is linked to the downregulation of key lipogenic regulators (SREBP1, PPAR-γ) and enzymes (FASN, ACC), alongside upregulated fatty acid oxidation (CPT1A). These findings elucidate how HS aggravates K. pneumoniae-induced mastitis by amplifying inflammation, disrupting barrier function, and inhibiting lactation, providing new insights into summer mastitis pathogenesis.

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Cite

BibTeXRIS
BibTeX
@article{guo2026heat,
  title = {{Heat stress enhances Klebsiella pneumoniae-induced cellular injury and impairs milk fat synthesis in bovine mammary epithelial cells}},
  author = {Jia Guo and Zhihao Wang and Haoran Zhong and Pengfei Dong and Kangjun Liu and Long Guo and Luying Cui and Junsheng Dong and Jianji Li and Guoqiang Zhu and Ran Wang and Lili Zhang and Xia Meng and Heng Wang},
  journal = {The Veterinary Quarterly},
  year = {2026},
  month = oct,
  doi = {10.1080/01652176.2026.2747449},
  url = {https://doi.org/10.1080/01652176.2026.2747449},
  note = {CC BY-NC 4.0},
}
RIS
TY  - JOUR
TI  - Heat stress enhances Klebsiella pneumoniae-induced cellular injury and impairs milk fat synthesis in bovine mammary epithelial cells
AU  - Jia Guo
AU  - Zhihao Wang
AU  - Haoran Zhong
AU  - Pengfei Dong
AU  - Kangjun Liu
AU  - Long Guo
AU  - Luying Cui
AU  - Junsheng Dong
AU  - Jianji Li
AU  - Guoqiang Zhu
AU  - Ran Wang
AU  - Lili Zhang
AU  - Xia Meng
AU  - Heng Wang
PY  - 2026
DA  - 2026/10/30
JO  - The Veterinary Quarterly
DO  - 10.1080/01652176.2026.2747449
UR  - https://doi.org/10.1080/01652176.2026.2747449
AB  - Heat stress (HS) poses a significant threat to dairy production by reducing milk yield and elevating the incidence of mastitis. Concurrently, mastitis caused by Klebsiella pneumoniae (K. pneumoniae) occurs more frequently during the summer months, further exacerbating udder health challenges. Our study demonstrates that combined HS and K. pneumoniae exposure significantly exacerbates cellular damage of bovine mammary epithelial cells (BMECs). Mechanistically, HS potentiates K. pneumoniae-induced NF-κB pathway activation and reactive oxygen species (ROS) accumulation, leading to upregulated pro-inflammatory cytokines, chemokines, and antimicrobial peptides. Simultaneously, HS disrupts tight junction integrity, downregulating ZO-1, Occludin, and Claudins, and compromises the epithelial barrier. Critically, HS further suppresses lipid accumulation and the expression of milk fat synthesis-related genes and proteins in K. pneumoniae-challenged BMECs. This metabolic suppression is linked to the downregulation of key lipogenic regulators (SREBP1, PPAR-γ) and enzymes (FASN, ACC), alongside upregulated fatty acid oxidation (CPT1A). These findings elucidate how HS aggravates K. pneumoniae-induced mastitis by amplifying inflammation, disrupting barrier function, and inhibiting lactation, providing new insights into summer mastitis pathogenesis.
SN  - 0165-2176
SN  - 1875-5941
ER  -