Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment.

Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment. Research Abstract Details 

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Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment. Abstract Text:

Ashok Kumar,Jia Yin,Jing Zhang,Fu-Shin X Yu,

PURPOSE: A prior study showed that Toll-like receptor (TLR)-5 recognizes Pseudomonas aeruginosa flagellin and triggers the production of proinflammatory cytokines in human corneal epithelial cells (HCECs). The present study was conducted to determine how the inflammatory response is modulated after TLR activation in HCECs. METHODS: HUCL cells, a telomerase-immortalized HCEC line, and primary cultures of HCECs were pretreated with low-dose flagellin and then challenged, with either a high dose of flagellin or with Pseudomonas. NF-kappaB activation was determined by the extent of IkappaB-alpha phosphorylation and degradation and of nuclear p65 DNA binding. The amount of cytokines in the culture media was assessed by ELISA. The activation of p38 and JNK and the cellular expression of TLR5 were determined by Western blot analysis. Cell surface distribution of TLR5 was assessed by flow cytometry. The expression and secretion of antimicrobial peptides were assessed by semiquantitative RT-PCR and slot-blot analysis, respectively. RESULTS: Pre-exposure (12-24 hours) of HCECs to low-dose flagellin induced a state of tolerance, characterized by impaired activation of the NF-kappaB, p38, and JNK pathways and reduced production of IL-8 and TNF-alpha on subsequent challenge with a high dose of flagellin. Flagellin-induced tolerance did not alter the cellular level and surface distribution of TLR5. Furthermore, flagellin priming of HCECs dampened the inflammatory response of HCECs to live Pseudomonas. Pseudomonas-induced upregulation of antimicrobial genes such as hBD2 and LL-37 was augmented, even in tolerized HCECs. CONCLUSIONS: Pre-exposure of the ocular surface to TLR agonists may induce protective mechanisms that not only modulate the host inflammatory response but also provide an innate defense against bacterial infection in the cornea.

Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment. Publishing Authors By Initials

A Kumar,J Yin,J Zhang,FS Yu,

For similar enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research abstracts see: enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research

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Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Investigative ophthalmology & visual science

VOLUME: 48

Page Numbers: 4664-70

Journal Abbreviation: Invest. Ophthalmol. Vis. Sci.

ISSN: 0146-0404

DAY: 3

MONTH: Oct

YEAR: 2007

Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment. Information

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LANGUAGE: eng

NlmUniqueID: 7703701

Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment. Keywords Mesh Terms:

KEYWORDS: p38 Mitogen-Activated Protein Kinases

MESH TERMS: metabolism

Chemical & Substance for Abstract: Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment. Information

Substance Name: p38 Mitogen-Activated Protein Kinases

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Modulation of corneal epithelial innate immune response to pseudomonas infection by flagellin pretreatment.

AFFILIATION: Kresge Eye Institute, Department of Ophthalmology, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.

Country: United States

AGENCY: United States NEI

GRANT: EY14080

ACRONYM: EY

MEDLINETA: Invest Ophthalmol Vis Sci

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