期刊
COMPARATIVE IMMUNOLOGY MICROBIOLOGY AND INFECTIOUS DISEASES
卷 34, 期 4, 页码 347-354出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.cimid.2011.04.004
关键词
Mastitis; Staphylococcus aureus; Innate immunity; IL-1 beta; Bovine mammary gland epithelial cells
资金
- Biogreen 21 Program
- Rural Development Administration [PJ007066]
- Korean Government (MEST) [2010-0029116, 20110001030]
- Ministry for Food, Agriculture, Forestry and Fisheries, Republic of Korea
- Institute of Planning & Evaluation for Technology in Food, Agriculture, Forestry & Fisheries (iPET), Republic of Korea [IPET710002-3] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2008-0062421] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Although mastitis caused by Staphylococcus aureus is a problematic inflammatory disease in lactating cows, the innate immunity to S. aureus in the mammary gland is poorly understood. In the present study, we observed that heat-killed S. aureus (HKS) induced IL-1 beta expression at both the mRNA and protein levels in the mammary gland epithelial cell-line, MAC-T. IL-1 beta production was suppressed by inhibitors of lipid rafts, ERK, JNK, and p38 kinases. Furthermore; HKS augmented the activities of the AP-1, CRE, and NF-kappa B transcription factors that regulate IL-1 beta gene expression. Among staphylococcal cell-wall components with inflammatory potential, Pam2CSK4 (a representative model for diacylated lipoproteins) enhanced IL-1 beta mRNA expression, while lipoteichoic acid and peptidoglycan did not. Collectively, we suggest that S. aureus-induced IL-1 beta production requires lipid raft formation, activation of MAP kinases, and activation of transcription factors AP-1, CRE, and NF-kappa B. Lipoprotein seems to be a major cell-wall component for the S. aureus-induced IL-1 beta production in bovine mammary gland epithelial cells. (C) 2011 Elsevier Ltd. All rights reserved.
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