| Staphylococcus aureus lipoproteins trigger human corneal epithelial innate response through toll-like receptor-2 | |
| Li, Qiong1,2; Kumar, Ashok1; Gui, Jian-Fang2; Yu, Fu-Shin X.1; Yu, FSX, Wayne State Univ, Sch Med, Dept Ophthalmol, Kresge Eye Inst, Detroit, MI 48201 USA | |
| 2008-05-01 | |
| Source Publication | MICROBIAL PATHOGENESIS
 |
| ISSN | 0882-4010 |
| Volume | 44Issue:5Pages:426-434 |
| Abstract | Bacterial lipoproteins (LP) are a family of cell wall components found in a wide variety of bacteria. In this study, we characterized the response of HUCL, a telomerase-immortalized human corneal epithelial cell (HCEC) line, to LP isolated from Staphylococcus (S) aureus. S. aureus LP (saLP) prepared by Triton X-114 extraction stimulated the activation of NF-kappa B, JNK, and P38 signaling pathways in HUCL cells. The extracts failed to stimulate NF-kappa B activation in HUCL cells after lipoprotein lipase treatment and in cell lines expressing TLR4 or TLR9, but not TLR2, indicating lipoprotein nature of the extracts. saLP induced the up-regulation of a variety of inflammatory cytokines and chemokines (IL-6, IL-8, ICAM-1). antimicrobial molecules (hBD-2, LL-37, and iNOS), and homeostasis genes (Mn-SOD) at both the mRNA level and protein level. Similar inflammatory response to saLP was also observed in primarily cultured HCECs using the production of IL-6 as readout. Moreover, TLR2 neutralizing antibody blocked the saLP-induced secretion of IL-6, IL-8 and hBD2 in HUCL cells. Our findings suggest that saLP activates TLR2 and triggers innate immune response in the cornea to S. aureus infection via production of proinflammatory cytokines and defense molecules. (C) 2007 Elsevier Ltd. All rights reserved.; Bacterial lipoproteins (LP) are a family of cell wall components found in a wide variety of bacteria. In this study, we characterized the response of HUCL, a telomerase-immortalized human corneal epithelial cell (HCEC) line, to LP isolated from Staphylococcus (S) aureus. S. aureus LP (saLP) prepared by Triton X-114 extraction stimulated the activation of NF-kappa B, JNK, and P38 signaling pathways in HUCL cells. The extracts failed to stimulate NF-kappa B activation in HUCL cells after lipoprotein lipase treatment and in cell lines expressing TLR4 or TLR9, but not TLR2, indicating lipoprotein nature of the extracts. saLP induced the up-regulation of a variety of inflammatory cytokines and chemokines (IL-6, IL-8, ICAM-1). antimicrobial molecules (hBD-2, LL-37, and iNOS), and homeostasis genes (Mn-SOD) at both the mRNA level and protein level. Similar inflammatory response to saLP was also observed in primarily cultured HCECs using the production of IL-6 as readout. Moreover, TLR2 neutralizing antibody blocked the saLP-induced secretion of IL-6, IL-8 and hBD2 in HUCL cells. Our findings suggest that saLP activates TLR2 and triggers innate immune response in the cornea to S. aureus infection via production of proinflammatory cytokines and defense molecules. (C) 2007 Elsevier Ltd. All rights reserved. |
| Subtype | Article |
| Keyword | Staphylococcus Aureus Toll-like Receptors Innate Resposne Lipoprotein Corneal Epithelium |
| Department | [Li, Qiong; Kumar, Ashok; Yu, Fu-Shin X.] Wayne State Univ, Sch Med, Dept Ophthalmol, Kresge Eye Inst, Detroit, MI 48201 USA; [Li, Qiong; Gui, Jian-Fang] Chinese Acad Sci, Inst Hydrobiol, Wuhan 430072, Peoples R China |
| Subject Area | Immunology ; Microbiology |
| DOI | 10.1016/j.micpath.2007.11.006 |
| WOS Headings | Science & Technology ; Life Sciences & Biomedicine |
| Funding Organization | NIH [R01EY14080, EY10869]; Research to Prevent Blindness to the Department of Ophthalmology, Wayne State University School of Medicine ; NIH [R01EY14080, EY10869]; Research to Prevent Blindness to the Department of Ophthalmology, Wayne State University School of Medicine ; NIH [R01EY14080, EY10869]; Research to Prevent Blindness to the Department of Ophthalmology, Wayne State University School of Medicine ; NIH [R01EY14080, EY10869]; Research to Prevent Blindness to the Department of Ophthalmology, Wayne State University School of Medicine |
| Indexed By | SCI |
| Language | 英语 |
| WOS Research Area | Immunology ; Microbiology |
| WOS Subject | Immunology ; Microbiology |
| WOS ID | WOS:000262591100008 |
| WOS Keyword | CELL-WALL COMPONENTS ; BACTERIAL KERATITIS ; HELICOBACTER-PYLORI ; LIPOTEICHOIC ACID ; SHIFTING TRENDS ; CUTTING EDGE ; PROTEIN-A ; PEPTIDOGLYCAN ; EXPRESSION ; INFECTION |
| Funding Organization | NIH [R01EY14080, EY10869]; Research to Prevent Blindness to the Department of Ophthalmology, Wayne State University School of Medicine ; NIH [R01EY14080, EY10869]; Research to Prevent Blindness to the Department of Ophthalmology, Wayne State University School of Medicine ; NIH [R01EY14080, EY10869]; Research to Prevent Blindness to the Department of Ophthalmology, Wayne State University School of Medicine ; NIH [R01EY14080, EY10869]; Research to Prevent Blindness to the Department of Ophthalmology, Wayne State University School of Medicine |
| Citation statistics | |
| Document Type | 期刊论文 |
| Identifier | http://ir.ihb.ac.cn/handle/152342/7906 |
| Collection | 期刊论文 |
| Corresponding Author | Yu, FSX, Wayne State Univ, Sch Med, Dept Ophthalmol, Kresge Eye Inst, Detroit, MI 48201 USA |
| Affiliation | 1.Wayne State Univ, Sch Med, Dept Ophthalmol, Kresge Eye Inst, Detroit, MI 48201 USA 2.Chinese Acad Sci, Inst Hydrobiol, Wuhan 430072, Peoples R China |
| Recommended Citation GB/T 7714 | Li, Qiong,Kumar, Ashok,Gui, Jian-Fang,et al. Staphylococcus aureus lipoproteins trigger human corneal epithelial innate response through toll-like receptor-2[J]. MICROBIAL PATHOGENESIS,2008,44(5):426-434. |
| APA | Li, Qiong,Kumar, Ashok,Gui, Jian-Fang,Yu, Fu-Shin X.,&Yu, FSX, Wayne State Univ, Sch Med, Dept Ophthalmol, Kresge Eye Inst, Detroit, MI 48201 USA.(2008).Staphylococcus aureus lipoproteins trigger human corneal epithelial innate response through toll-like receptor-2.MICROBIAL PATHOGENESIS,44(5),426-434. |
| MLA | Li, Qiong,et al."Staphylococcus aureus lipoproteins trigger human corneal epithelial innate response through toll-like receptor-2".MICROBIAL PATHOGENESIS 44.5(2008):426-434. |
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