IL-1ß induces increased tight junction permeability in bovine mammary epithelial cells via the IL-1ß-ERK1/2-MLCK axis upon blood-milk barrier damage.
J Cell Biochem
; 119(11): 9028-9041, 2018 11.
Article
em En
| MEDLINE
| ID: mdl-30011095
ABSTRACT
Bovine mastitis occurs frequently in dairy cows and is often caused by various aetiological organisms, for example, Escherichia coli. Lipopolysaccharide (LPS) is a key virulence factor of E. coli. In this study, we stimulated bovine mammary epithelial cells (BMECs) with LPS to investigate the global transcriptional response and identify specific proinflammatory factors that play important roles in blood-milk barrier damage during mastitis caused by E. coli. By performing RNA-seq, we identified a large number of significantly differentially expressed genes (DEGs) between the LPS-treated BMECs and the control cells. Among the DEGs, interleukin-1ß (IL-1ß) was selected because its messenger RNA expression was induced by LPS and its enrichment is involved in multiple inflammatory signal pathways, and its roles in blood-milk barrier damage during the process of mastitis were investigated. Exogenous IL-1ß treatment damaged the integrity of the blood-milk barrier, as indicated by the increased BMEC tight junction (TJ) permeability and confirmed by in vitro and in vivo experiments. Furthermore, the IL-1ß-induced increase in the BMEC TJ permeability was mediated by the IL-1ß-ERK1/2-MLCK axis pathway. Our data provide insights into the functions of IL-1ß in blood-milk barrier damage caused by mastitis in dairy cows.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Junções Íntimas
/
Proteína Quinase 1 Ativada por Mitógeno
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Proteína Quinase 3 Ativada por Mitógeno
/
Células Epiteliais
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Interleucina-1beta
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Glândulas Mamárias Animais
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article