Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3201141 | Journal of Allergy and Clinical Immunology | 2009 | 17 Pages |
Abstract
NO inhibits HRV-16-induced production of CXCL10 by inhibiting viral activation of nuclear factor κB and of IRFs, including IRF-1, through a cGMP-independent pathway. The broad-ranging inhibition of HRV-induced epithelial cytokine and chemokine production by NO suggests a potential therapeutic utility of NO donors in viral exacerbations of asthma and chronic obstructive pulmonary disease.
Keywords
NF-κBODQBEGMCXCL10ISREIRFdsRNAHBEIKKβTCIDAP-1PMSFGAPDHcGMPISGFiNOS1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-oneHRVdouble-stranded RNAElectrophoretic mobility shift assayAsthmaCOPDChronic obstructive pulmonary diseaseTissue culture infective doseHuman rhinovirusairway epithelial cellinducible nitric oxide synthaseEMSA یا electrophoretic mobility shift assay IFN regulatory factorIFN-stimulated response elementnuclear factor κBphenylmethylsulfonyl fluoridecyclic guanosine monophosphateNitric oxideactivator protein 1glyceraldehyde-3-phosphate dehydrogenase
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Authors
Rommy MD, MSc, Raza S. BSc, Shahina MSc, Neil S. PhD, Mark A. PhD, David PhD,