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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 PublicationMICROBIAL PATHOGENESIS
ISSN0882-4010
Volume44Issue:5Pages:426-434
AbstractBacterial 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.
SubtypeArticle
KeywordStaphylococcus 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 AreaImmunology ; Microbiology
DOI10.1016/j.micpath.2007.11.006
WOS HeadingsScience & Technology ; Life Sciences & Biomedicine
Funding OrganizationNIH [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 BySCI
Language英语
WOS Research AreaImmunology ; Microbiology
WOS SubjectImmunology ; Microbiology
WOS IDWOS:000262591100008
WOS KeywordCELL-WALL COMPONENTS ; BACTERIAL KERATITIS ; HELICOBACTER-PYLORI ; LIPOTEICHOIC ACID ; SHIFTING TRENDS ; CUTTING EDGE ; PROTEIN-A ; PEPTIDOGLYCAN ; EXPRESSION ; INFECTION
Funding OrganizationNIH [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
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Cited Times:43[WOS]   [WOS Record]     [Related Records in WOS]
Document Type期刊论文
Identifierhttp://ir.ihb.ac.cn/handle/152342/7906
Collection期刊论文
Corresponding AuthorYu, FSX, Wayne State Univ, Sch Med, Dept Ophthalmol, Kresge Eye Inst, Detroit, MI 48201 USA
Affiliation1.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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