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IL-8 EXPRESSION IN NORMAL NASAL EPITHELIUM AND ITS MODULATION BY INFECTION WITH RESPIRATORY SYNCYTIAL VIRUS AND CYTOKINES TNF, IL-1, AND IL-6
Citation:
Becker, S., H. Koren, AND D. Henke. IL-8 EXPRESSION IN NORMAL NASAL EPITHELIUM AND ITS MODULATION BY INFECTION WITH RESPIRATORY SYNCYTIAL VIRUS AND CYTOKINES TNF, IL-1, AND IL-6. U.S. Environmental Protection Agency, Washington, D.C., EPA/600/J-93/098.
Description:
Inflammation in the nasal and airway tissue caused by allergens, microbial infection and air pollution is likely to be regulated by inflammatory mediators produced by airway epithelial cells. We have therefore investigated the baseline expression of a number of cytokine genes known to be important inducers and modulators of inflammation, in freshly isolated human nasal epithelium. Cells were obtained by superficial scraping of turbinate tissue and cDNA for PCR amplification was reverse transcribed directly from lysates of 3-5 x 10 3 epithelial cells using random hexamers. Constitutive expression of high levels of IL-8 mRNA but undetectable levels of GM-CSF, IL-l or TNF mRNA were found after PCR amplification of the cDNA. However, amplification of cytokine cDNAs reverse transcribed from purified RNA from pool scrapings of 8 subjects (approximately 100 x the amount of cDNA/PCR assay) revealed low level expression of TNF, IL-6 and GM-CSF, IL-beta but not of IL-1 alpha mRNA. Infection with respiratory syncytial virus (RSV) or stimulation of nasal epithelium for 4 hours with TNF or IL-1 in vitro, resulted in a 4 to 10 fold increase in IL-8 mRNA expression but not in the expression of detectable levels of mRNA for the other cytokines. IL-8 protein was released both by RSV-, IL-1, and TNF-stimulated, as well as unstimulated, nasal epithelial cells after 6 to 20 hours of culture, while neither IL-6 nor TNF activity was detectable. Thus, it appears that IL-8 is a major cytokine of human nasal epithelium, constitutively expressed and readily secreted upon virus infection or stimulation with IL-1 and TNF.