Staphylococcus aureus protein A induced inflammatory response in human corneal epithelial cells |
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Authors: | Kumar Ashok Tassopoulos Alexander Mark Li Qiong Yu Fu-Shin X |
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Affiliation: | The Kresge Eye Institute, Department of Ophthalmology, Wayne State University School of Medicine, Detroit, MI 48201, USA. akuma@med.wayne.edu |
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Abstract: | In the present study, we examined the role of Staphylococcus aureus protein A (SpA) in inducing inflammatory response in human corneal epithelial cells (HCECs). Exposure of HCECs to SpA induces rapid NF-kappaB activation and secretion of proinflammatory cytokine/chemokines (TNF-alpha and IL-8) in both concentration and time-dependent manner. Challenge of HCECs with live SpA(-/-) mutant S. aureus strains resulted in significantly reduced production of the cytokines when compared to the wild-type S. aureus strain. SpA also elicited the activation of MAP Kinases P38, ERK, but not JNK, in HCECs. SpA-induced production of proinflammatory cytokine were completely blocked by the NF-kappaB and p38 inhibitors and partially inhibited by the Jnk inhibitor. Pretreatment with anti-TLR2 neutralizing antibody had no effect on SpA-induced inflammatory response in HCECs, suggesting that this response is independent of TLR2 signaling. Moreover, unlike TLR2 ligands, SpA failed to induce the expression of antimicrobial peptides (hBD2 and LL-37) in HCECs. These studies indicate that SpA is a S. aureus virulence factor that stimulates HCEC inflammatory response through a pathway distinct from TLR2 in HCECs. |
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Keywords: | Staphylococcus aureus Staphylococcal protein A Inflammation Toll-like receptors Keratitis Corneal epithelial cells Eye Cornea Cytokine |
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