{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T20:20:29Z","timestamp":1790626829139,"version":"4.1.0"},"reference-count":37,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2001,1,1]],"date-time":"2001-01-01T00:00:00Z","timestamp":978307200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2001,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Eotaxin is a potent eosinophil chemoattractant that contributes to the eosinophilia seen in asthma and other allergic disorders. Recent studies have identified human airway smooth muscle (HASM) as a rich source of eotaxin, but the factors regulating its production are poorly understood. Here we describe for the first time that \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010agonists can inhibit cytokineinduced eotaxin release. We found that TNF\u2010\u03b1 stimulated eotaxin release (assayed by ELISA) from HASM cells and that the release was partially inhibited by salbutamol and salmeterol. The effect of \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010agonists was mimicked by forskolin and 8\u2010bromo\u2010cAMP and potentiated by the cAMP\u2010dependent phosphodiesterase inhibitor rolipram, suggesting that it is cAMP dependent. We also found that the cAMP inhibition was likely at the transcription stage, although experiments with the PKA inhibitors H\u201089 and Rp\u2010cAMP or the PKG inhibitor KT5823 suggested that none of these kinases was involved. Partial inhibition of eotaxin release was also seen with the corticosteroids dexamethasone and fluticasone. The combined use of \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010agonists, rolipram, and steroids abolished TNF\u2010\u03b1\u2010induced eotaxin release. These results suggest that the combination of a \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010agonist, PDE inhibitor, and a corticosteroid may have additive beneficial effects in the treatment of the eosinophilia associated with asthma and other allergic diseases\u2014Pang, L., Knox, A. J. Regulation of TNF\u2010\u03b1\u2010induced eotaxin release from cultured human airway smooth muscle cells by \u03b2\n                    <jats:sub>2<\/jats:sub>\n                    \u2010agonists and corticosteroids.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    15, 261\u2013269 (2001)\n                  <\/jats:p>","DOI":"10.1096\/fj.00-0103com","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T19:03:10Z","timestamp":1027710190000},"page":"261-269","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":118,"title":["Regulation of TNF\u2010\u03b1\u2010induced eotaxin release from cultured human airway smooth muscle cells by \u03b2\n                    <sub>2<\/sub>\n                    \u2010agonists and corticosteroids"],"prefix":"10.1096","volume":"15","author":[{"given":"LINHUA","family":"PANG","sequence":"first","affiliation":[{"name":"Division of Respiratory Medicine City Hospital University of Nottingham  Nottingham U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"ALAN J.","family":"KNOX","sequence":"additional","affiliation":[{"name":"Division of Respiratory Medicine City Hospital University of Nottingham  Nottingham U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2001,1]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.179.3.881"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/nm0496-449"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI118456"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.92.19.8960"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1007\/BF03401631"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119624"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6100"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.277.5334.2005"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.159.9.4593"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1164\/ajrccm.159.6.9805039"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.6958"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830271252"},{"key":"e_1_2_7_14_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2249.1998.00688.x"},{"key":"e_1_2_7_15_1","doi-asserted-by":"publisher","DOI":"10.1165\/ajrcmb.17.6.2865"},{"key":"e_1_2_7_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/0091-6749(91)90125-8"},{"key":"e_1_2_7_17_1","doi-asserted-by":"publisher","DOI":"10.1016\/0091-6749(92)90218-Q"},{"key":"e_1_2_7_18_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI119341"},{"key":"e_1_2_7_19_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.bjp.0702660"},{"key":"e_1_2_7_20_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.271.13.7725"},{"key":"e_1_2_7_21_1","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1997.7169"},{"key":"e_1_2_7_22_1","doi-asserted-by":"crossref","first-page":"3189","DOI":"10.4049\/jimmunol.137.10.3189","article-title":"Prostaglandins posttranscriptionally inhibit monocyte expression of interleukin 1 activity by increasing intracellular cyclic adenosine monophosphate","volume":"137","author":"Knudsen P. 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