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Recently, interleukin (IL)-16 (lymphocyte chemoattractant factor) was reported to be a potent chemotactic stimulus for CD4+ T lymphocytes and eosinophils, the types of leukocyte found in the proximity of bronchial epithelium in asthmatic individuals. To test the possibility that bronchial epithelial cells produce IL-16, we analyzed RNA and culture supernatants from the human bronchial epithelial cell line BEAS-2B, using reverse transcription\u2013polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. BEAS-2B constitutively expressed IL-16 messenger RNA (mRNA) and protein; IL-16 expression was significantly upregulated in a concentration-dependent manner within 24 h by stimulation with histamine, IL-1\u03b2, or tumor necrosis factor (TNF)-\u03b1 whereas interferon-\u03b3 did not significantly increase IL-16. Findings in BEAS-2B cells were confirmed in primary bronchial epithelial cells. Using TA cloning, IL-16 was cloned from BEAS-2B airway epithelial cells. Sequence analysis confirmed its near identity with lymphocyte-derived IL-16. The combination of IL-1\u03b2 and TNF-\u03b1 had an additive effect on IL-16 expression. This combination of cytokines also had a priming effect on histamine-induced IL-16 mRNA expression, which was observed within 24 h and which increased to at least 48 h after stimulation. The IL-16 expression induced by histamine and combined cytokines was significantly inhibited by pretreatment with the protein synthesis inhibitor cycloheximide (10 \u03bcg\/ml). Pretreatment with dexamethasone also significantly suppressed the expression of IL-16, in a concentration-dependent manner. Sputum samples from asthmatic subjects were found to have higher levels of IL-16 than were samples from subjects with other pulmonary inflammatory diseases. These findings suggest that bronchial epithelial cells have the capacity to produce IL-16 after stimulation with histamine, IL-1\u03b2, and TNF-\u03b1, and raise the possibility that epithelium-derived IL-16 may play a role in recruitment of eosinophils and CD4+ T lymphocytes in the airways. Downregulation of IL-16 expression by dexamethasone suggests that glucocorticoids may inhibit airway inflammation partly by suppressing the synthesis of inflammatory cytokines including IL-16.<\/jats:p>","DOI":"10.1165\/ajrcmb.21.6.3671","type":"journal-article","created":{"date-parts":[[2013,4,3]],"date-time":"2013-04-03T22:05:27Z","timestamp":1365026727000},"page":"684-692","source":"Crossref","is-referenced-by-count":49,"title":["Expression of Interleukin-16 by Human Epithelial Cells: Inhibition by Dexamethasone"],"prefix":"10.1093","volume":"21","author":[{"given":"Masafumi","family":"Arima","sequence":"first","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dokkyo University School of Medicine, Mibu, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jim","family":"Plitt","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dokkyo University School of Medicine, Mibu, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cristiana","family":"Stellato","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dokkyo University School of Medicine, Mibu, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carol","family":"Bickel","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dokkyo University School of Medicine, Mibu, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shinji","family":"Motojima","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dokkyo University School of Medicine, Mibu, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sohei","family":"Makino","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dokkyo University School of Medicine, Mibu, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takeshi","family":"Fukuda","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dokkyo University School of Medicine, Mibu, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Robert P.","family":"Schleimer","sequence":"additional","affiliation":[{"name":"Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Dokkyo University School of Medicine, Mibu, Tochigi, Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[1999,12,1]]},"reference":[{"key":"2026030700100674700_B1"},{"key":"2026030700100674700_B2","doi-asserted-by":"crossref","first-page":"970","DOI":"10.1164\/ajrccm\/141.4_Pt_1.","article-title":"CD4 T-lymphocyte activation in acute severe asthma: relationship to disease severity and atopic status.","volume":"141","author":"Corrigan","year":"1990","journal-title":"Am. 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