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Because airway epithelium is an important cellular source of inflammatory mediators, the objective of the present study was to determine whether adenosine affects the expression and release of inflammatory cytokines from human bronchial epithelial cells (HBECs). Among the four subtypes of adenosine receptors, the A2B receptor was expressed at the highest level. 5\u2032-(N-ethylcarboxamido)-adenosine (NECA), a stable analog of adenosine, increased the release of IL-19 by 4.6- \u00b1 1.1-fold. A selective antagonist of the A2B receptor, CVT-6694, attenuated this effect of NECA. The amount of IL-19 released from HBEC was sufficient to activate a human monocytic cell line (THP-1) and increase the release of TNF-\u03b1. Furthermore, TNF-\u03b1 was found to upregulate A2B receptor expression in HBECs by 3.1- \u00b1 0.3-fold. Hence, these data indicate that NECA increases the release of IL-19 from HBECs via activation of A2B receptors, and IL-19 in turn activates human monocytes to release TNF-\u03b1, which upregulates A2B receptor expression in HBECs. The results of this study suggest that there is a novel pathway whereby adenosine can initiate and amplify an inflammatory response which might be important in pathogenesis of inflammatory lung diseases.<\/jats:p>","DOI":"10.1165\/rcmb.2005-0476oc","type":"journal-article","created":{"date-parts":[[2006,6,15]],"date-time":"2006-06-15T21:16:14Z","timestamp":1150406174000},"page":"587-592","source":"Crossref","is-referenced-by-count":89,"title":["A2B Adenosine Receptors Induce IL-19 from Bronchial Epithelial Cells, Resulting in TNF-\u03b1 Increase"],"prefix":"10.1093","volume":"35","author":[{"given":"Hongyan","family":"Zhong","sequence":"first","affiliation":[{"name":"Department of Drug Research and Pharmacological Sciences, CV Therapeutics, Inc., Palo Alto, California"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuzhi","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Drug Research and Pharmacological Sciences, CV Therapeutics, Inc., Palo 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