Publication:
Influence of lipopolysaccharide on proinflammatory gene expression in human corneal, conjunctival and meibomian gland epithelial cells

dc.contributor.coauthorChen, Di
dc.contributor.coauthorKam, Wendy R.
dc.contributor.coauthorLiu, Yang
dc.contributor.coauthorDarabad, Raheleh Rahimi
dc.contributor.coauthorSullivan, David A.
dc.contributor.kuauthorŞahin, Afsun
dc.contributor.kuprofileFaculty Member
dc.contributor.schoolcollegeinstituteSchool of Medicine
dc.contributor.yokid171267
dc.date.accessioned2024-11-09T23:25:51Z
dc.date.issued2018
dc.description.abstractPurpose: Lipopolysaccharide (LPS), a bacterial endotoxin, is known to stimulate leuokotriene B4 (LTB4) secretion by human corneal (HCECs), conjunctival (HConjECs) and meibomian gland (HMGECs) epithelial cells. We hypothesize that this LTB4 effect represents an overall induction of proinflammatory gene expression in these cells. Our objective was to test this hypothesis. Methods: Immortalized HCECs, HConjECs and HMGECs were cultured in the presence or absence of LPS (15 mu g/ ml) and ligand binding protein (LBP; 150 ng/ml). Cells were then processed for RNA isolation and the analysis of gene expression by using Illumina BeadChips, background subtraction, cubic spline normalization and GeneSifter software. Results: Our findings show that LPS induces a striking increase in proinflammatory gene expression in HCECs and HConjECs. These cellular reactions are associated with a significant up-regulation of genes associated with inflammatory and immune responses (e.g. IL-15, IL-8, and tumor necrosis factor), including those related to chemokine and Toll-like receptor signaling pathways, cytokine-cytokine receptor interactions, and chemotaxis. In contrast, with the exception of Toll-like signaling and associated innate immunity pathways, almost no proinflammatory ontologies were upregulated by LPS in HMGECs. Conclusions: Our results support our hypothesis that LPS stimulates proinflammatory gene expression in HCECs and HConjECs. However, our findings also show that LPS does not elicit such proinflammatory responses in HMGECs.
dc.description.indexedbyWoS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue3
dc.description.openaccessYES
dc.description.publisherscopeInternational
dc.description.sponsoredbyTubitakEuN/A
dc.description.sponsorshipNIH [EY05612]
dc.description.sponsorshipMargaret S. Sinon Scholar in Ocular Surface Research fund
dc.description.sponsorshipARVO/Pfizer
dc.description.sponsorshipTUBITAK
dc.description.sponsorshipOne-Hundred-Talent Scholarship Program of Peking Union Medical College Hospital
dc.description.sponsorshipGuoxing Yao Research Fund Supported by NIH grant EY05612, the Margaret S. Sinon Scholar in Ocular Surface Research fund, ARVO/Pfizer, TUBITAK, the One-Hundred-Talent Scholarship Program of Peking Union Medical College Hospital, and the Guoxing Yao Research Fund.
dc.description.volume16
dc.identifier.doi10.1016/j.jtos.2018.05.003
dc.identifier.eissn1937-5913
dc.identifier.issn1542-0124
dc.identifier.quartileQ1
dc.identifier.scopus2-s2.0-85046870346
dc.identifier.urihttp://dx.doi.org/10.1016/j.jtos.2018.05.003
dc.identifier.urihttps://hdl.handle.net/20.500.14288/11453
dc.identifier.wos436496600016
dc.keywordsLipopolysaccharide
dc.keywordsInflammation
dc.keywordsGene expression
dc.keywordsOcular surface epithelial cells
dc.languageEnglish
dc.publisherElsevier
dc.sourceOcular Surface
dc.subjectOphthalmology
dc.titleInfluence of lipopolysaccharide on proinflammatory gene expression in human corneal, conjunctival and meibomian gland epithelial cells
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.authorid0000-0002-5083-5618
local.contributor.kuauthorŞahin, Afsun

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