Staphylococcus aureus induces IL-1β expression through the activation of MAP kinases and AP-1, CRE and NF-κB transcription factors in the bovine mammary gland epithelial cells

• Published in: Comparative immunology, microbiology and infectious diseases Vol. 34; no. 4; pp. 347 - 354
• Main Authors: Kim, Kyoung Whun, Im, Jintaek, Jeon, Jun Ho, Lee, Hong-Gu, Yun, Cheol-Heui, Han, Seung Hyun
• Format: Journal Article
• Language: English
• Published: Kidlington Elsevier Ltd 01.07.2011; Elsevier
• Subjects: Allergy and Immunology; Animals; Antigens, Bacterial - immunology; Antigens, Bacterial - pharmacology; Bacteriology; Biological and medical sciences; Bovine mammary gland epithelial cells; Cattle; Cell Line; Epithelial Cells - cytology; Epithelial Cells - immunology; Epithelial Cells - metabolism; Female; Fundamental and applied biological sciences. Psychology; Gene Expression; Hot Temperature; IL-1β; Immunity, Innate; Infectious Disease; Innate immunity; Interleukin-1beta - agonists; Interleukin-1beta - antagonists & inhibitors; Interleukin-1beta - biosynthesis; JNK Mitogen-Activated Protein Kinases - genetics; JNK Mitogen-Activated Protein Kinases - immunology; JNK Mitogen-Activated Protein Kinases - metabolism; Lipopeptides - pharmacology; Mammary Glands, Animal - cytology; Mammary Glands, Animal - immunology; Mammary Glands, Animal - metabolism; Mammary Glands, Animal - microbiology; Mastitis; Membrane Microdomains - drug effects; Membrane Microdomains - metabolism; Microbiology; Miscellaneous; Mitogen-Activated Protein Kinases - genetics; Mitogen-Activated Protein Kinases - immunology; Mitogen-Activated Protein Kinases - metabolism; NF-kappa B - genetics; NF-kappa B - immunology; NF-kappa B - metabolism; p38 Mitogen-Activated Protein Kinases - genetics; p38 Mitogen-Activated Protein Kinases - immunology; p38 Mitogen-Activated Protein Kinases - metabolism; Protein Kinase Inhibitors - pharmacology; RNA, Messenger - analysis; Signal Transduction - genetics; Signal Transduction - immunology; Staphylococcal Infections - immunology; Staphylococcal Infections - metabolism; Staphylococcal Infections - microbiology; Staphylococcal Infections - prevention & control; Staphylococcus aureus; Staphylococcus aureus - growth & development; Transcription Factor AP-1 - genetics; Transcription Factor AP-1 - immunology; Transcription Factor AP-1 - metabolism; Transcription Factor RelA - genetics; Transcription Factor RelA - immunology; Transcription Factor RelA - metabolism; Vaccination; Vaccines, Attenuated - administration & dosage; extracellular signal-regulated kinase; JNK; Innate immunity; real-time RT-PCR; AP-1; LPS; mitogen-activated protein kinase; NF-κB; CFU; interleukin; Staphylococcus aureus; c-Jun N-terminal kinase; Mastitis; IL; cyclic AMP-responsive element; Bovine mammary gland epithelial cells; MAP kinase; nuclear factor-kappa B; real-time reverse transcription polymerase chain reaction; IL-1β; peptidoglycan; TNF-α; colony forming unit; PGN; tumor necrosis factor-α; CRE; enzyme-linked immunosorbent assay; LTA; lipoteichoic acid; activating protein 1; lipopolysaccharide; ELISA; ERK; Natural immunity; Immunology; Bacteria; Micrococcales; Micrococcaceae; Transcription factor NFκB; Mammary gland; Transcription factor; Ungulata; Bovine; Enzyme; Transferases; Cytokine; Mitogen-activated protein kinase; Interleukin 1β; Response element; Infection; Mammary gland diseases; Vertebrata; Mammalia; Epithelial cell; Artiodactyla; Veterinary
• ISSN: 0147-9571; 1878-1667
• DOI: 10.1016/j.cimid.2011.04.004

Abstract 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-1β expression at both the mRNA and protein levels in the mammary gland epithelial cell-line, MAC-T. IL-1β 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-κB transcription factors that regulate IL-1β gene expression. Among staphylococcal cell-wall components with inflammatory potential, Pam2CSK4 (a representative model for diacylated lipoproteins) enhanced IL-1β mRNA expression, while lipoteichoic acid and peptidoglycan did not. Collectively, we suggest that S. aureus -induced IL-1β production requires lipid raft formation, activation of MAP kinases, and activation of transcription factors AP-1, CRE, and NF-κB. Lipoprotein seems to be a major cell-wall component for the S. aureus -induced IL-1β production in bovine mammary gland epithelial cells.