{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T04:41:55Z","timestamp":1774932115378,"version":"3.50.1"},"reference-count":63,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Lung Cellular and Molecular Physiology"],"published-print":{"date-parts":[[2008,2]]},"abstract":"<jats:p>CD38 is involved in normal airway function, IL-13-induced airway hyperresponsiveness (AHR), and is also regulated by tumor necrosis factor (TNF)-\u03b1 in airway smooth muscle (ASM) cells. This study aimed to determine whether TNF-\u03b1-induced CD38 upregulation in ASM cells contributes to AHR, a hallmark of asthma. We hypothesized that AHR would be attenuated in TNF-\u03b1-exposed CD38-deficient (CD38KO) mice compared with wild-type (WT) controls. Mice ( n = 6\u20138\/group) were intranasally challenged with vehicle control or TNF-\u03b1 (50 ng) once and every other day during 1 or 4 wk. Lung inflammation and AHR, measured by changes in lung resistance after inhaled methacholine, were assessed 24 h following the last challenge. Tracheal rings were incubated with TNF-\u03b1 (50 ng\/ml) to assess contractile changes in the ASM. While a single TNF-\u03b1 challenge caused no airway inflammation, both multiple-challenge protocols induced equally significant inflammation in CD38KO and WT mice. A single intranasal TNF-\u03b1 challenge induced AHR in the WT but not in the CD38KO mice, whereas both mice developed AHR after 1 wk of challenges. The AHR was suppressed by extending the challenges for 4 wk in both mice, although to a larger magnitude in the WT than in the CD38KO mice. TNF-\u03b1 increased ASM contractile properties in tracheal rings from WT but not from CD38KO mice. In conclusion, CD38 contributes to TNF-\u03b1-induced AHR after a brief airway exposure to the cytokine, likely by mediating changes in ASM contractile responses, and is associated with greater AHR remission following chronic airway exposure to TNF-\u03b1. The mechanisms involved in this remission remain to be determined.<\/jats:p>","DOI":"10.1152\/ajplung.00367.2007","type":"journal-article","created":{"date-parts":[[2007,12,1]],"date-time":"2007-12-01T01:54:32Z","timestamp":1196474072000},"page":"L290-L299","source":"Crossref","is-referenced-by-count":49,"title":["Role of CD38 in TNF-\u03b1-induced airway hyperresponsiveness"],"prefix":"10.1152","volume":"294","author":[{"given":"Alonso G. 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