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Accordingly, we investigated the effect of T-helper 1 (TH1) and 2 (TH2) cytokines and the anti-inflammatory agents fluticasone and salmeterol on HA synthesis in human lung fibroblasts. Interleukin-1\u03b2 (IL-1\u03b2) and tumor necrosis factor (TNF)-\u03b1 were the most potent stimulators of HA synthesis and when combined, caused synergistic increases in HA accumulation. Time-course analysis of HA accumulation and [3H]-glucosamine incorporation into HA demonstrated continued synthesis over the 24 h of stimulation. Peak synthesis at 6\u201312 h coincided with an increased proportion of high molecular weight HA. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that IL-1\u03b2 and TNF-\u03b1 induced HA synthase-2 messenger RNA (mRNA) 3 h following stimulation and remained elevated throughout the 24-h stimulation period. Fluticasone inhibited IL-1\u03b2 and TNF-\u03b1 induced HA synthesis (44.5%) whereas salmeterol had no effect. When combined, fluticasone and salmeterol inhibited HA synthesis to a greater extent (85.2%). Further, fluticasone attenuated IL-1\u03b2 and TNF-\u03b1 stimulated hyaluronan synthase-2 messenger RNA (mRNA), and the addition of salmeterol cooperatively enhanced this inhibition. These results indicate that enhanced synthesis of HA by the proinflammatory cytokines IL-1\u03b2 and TNF-\u03b1 can be abrogated by specific corticosteroid and \u03b22 blocker combinations shown to be effective in the treatment of asthma.<\/jats:p>","DOI":"10.1165\/rcmb.2003-0380oc","type":"journal-article","created":{"date-parts":[[2004,2,9]],"date-time":"2004-02-09T20:24:49Z","timestamp":1076358289000},"page":"92-99","source":"Crossref","is-referenced-by-count":91,"title":["Pro- and Anti-Inflammatory Factors Cooperate to Control Hyaluronan Synthesis in Lung Fibroblasts"],"prefix":"10.1093","volume":"31","author":[{"given":"Thomas S.","family":"Wilkinson","sequence":"first","affiliation":[{"name":"Department of Vascular Biology, Hope Heart Institute, Seattle; and Department of Medicine, Division of Allergy and Infectious Disease, and Department of Pathology, University of Washington, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan","family":"Potter-Perigo","sequence":"additional","affiliation":[{"name":"Department of Vascular Biology, Hope Heart Institute, Seattle; and Department of Medicine, Division of Allergy and Infectious Disease, and Department of Pathology, University of Washington, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Tsoi","sequence":"additional","affiliation":[{"name":"Department of Vascular Biology, Hope Heart Institute, Seattle; and Department of Medicine, Division of Allergy and Infectious Disease, and Department of Pathology, University of Washington, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leonard C.","family":"Altman","sequence":"additional","affiliation":[{"name":"Department of Vascular Biology, Hope Heart Institute, Seattle; and Department of Medicine, Division of Allergy and Infectious Disease, and Department of Pathology, University of Washington, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas N.","family":"Wight","sequence":"additional","affiliation":[{"name":"Department of Vascular Biology, Hope Heart Institute, Seattle; and Department of Medicine, Division of Allergy and Infectious Disease, and Department of Pathology, University of Washington, Seattle, Washington"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2004,7,1]]},"reference":[{"key":"2026030623463651200_BIB1","doi-asserted-by":"crossref","first-page":"1001","DOI":"10.1172\/JCI8124","volume":"104","year":"1999","journal-title":"J. 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