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Toll-like receptor 4 initiates an innate immune response to lipopolysaccharide in human conjunctival epithelial cells.

Authors
 So-Hyang Chung  ;  Mi-Na Kweon  ;  Hyung Keun Lee  ;  Seung-Il Choi  ;  Jin-Young Yang  ;  Eung Kweon Kim 
Citation
 EXPERIMENTAL EYE RESEARCH, Vol.88(1) : 49-56, 2009 
Journal Title
 EXPERIMENTAL EYE RESEARCH 
ISSN
 0014-4835 
Issue Date
2009
MeSH
Cells, Cultured ; Conjunctiva/immunology* ; Cytokines/biosynthesis ; Dose-Response Relationship, Immunologic ; Epithelial Cells/immunology ; Eye Proteins/genetics ; Eye Proteins/immunology* ; Gene Expression/immunology ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Inflammation/immunology ; Intracellular Signaling Peptides and Proteins/immunology ; Lipopolysaccharide Receptors/biosynthesis ; Lipopolysaccharide Receptors/genetics ; Lipopolysaccharides/immunology ; NF-kappa B/immunology ; Neoplasm Proteins/immunology ; RNA, Messenger/genetics ; Reverse Transcriptase Polymerase Chain Reaction/methods ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/immunology*
Keywords
conjunctival epithelial cells ; innate immune response ; IL-6 ; IL-8 ; toll-like receptor 4
Abstract
Conjunctival epithelial cells serve as a first line of defense against pathogens presented to the innate immune system. The inflammatory response to Gram-negative bacteria is initiated by toll-like receptor 4 (TLR4). This study investigated whether a TLR4 ligand induces production of inflammatory cytokines in human conjunctival epithelial cells (HCECs) through nuclear factor kappa-B (NF-kappaB). HCECs were evaluated for TLR4 expression by reverse transcriptase-polymerase chain reaction, Western blot analysis, and flow cytometric analysis. HCECs were stimulated with various concentrations of lipopolysaccharide (LPS) and the innate immune response was quantified by measuring expression of the inflammatory cytokines IL-6 and IL-8. Functional NF-kappaB activation was examined using a luciferase reporter assay. Expression of TLR4-specific mRNA as well as its corresponding protein was observed in HCECs. Surface and intracellular expression of TLR4 was observed in flow cytometric analysis. Incubation of HCECs with LPS led to secretion of IL-6 and IL-8. Blockade of TLR4- and TNFR-associated factor (TRAF) 6 activity abolished LPS-induced inflammatory response in HCECs and incubation of HCECs with LPS led to activation of the NF-kappaB transcription factor. LPS did not enhance the TLR4 expression at both mRNA and protein levels in HCECs. Our results demonstrate that surface expression of TLR4 in HCECs can elicit a TLR4-mediated innate immune response through TRAF6-NF-kappaB and contribute to an inflammatory environment on the ocular surface.
Full Text
http://www.sciencedirect.com/science/article/pii/S001448350800328X
DOI
10.1016/j.exer.2008.09.017
Appears in Collections:
5. Research Institutes (연구소) > Corneal Dystrophy Research Institute (각막이상증연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Eung Kweon(김응권) ORCID logo https://orcid.org/0000-0002-1453-8042
Lee, Hyung Keun(이형근) ORCID logo https://orcid.org/0000-0002-1123-2136
Choi, Seung Il(최승일) ORCID logo https://orcid.org/0000-0001-7168-8795
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/103391
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