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Exposure of bronchial epithelial cells to aqueous extracts of hog CAFO dusts (HDE) leads to inflammatory cytokine production that is driven by protein kinase C (PKC) activation. cAMP-dependent protein kinase (PKA)-activating agents can inhibit PKC activation in epithelial cells, leading to reduced inflammatory cytokine production following HDE exposure. \u03b2<jats:sub>2<\/jats:sub>-Adrenergic receptor agonists (\u03b2<jats:sub>2<\/jats:sub>-agonists) activate PKA, and we hypothesized that \u03b2<jats:sub>2<\/jats:sub>-agonists would beneficially impact HDE-induced adverse airway inflammatory consequences. Bronchial epithelial cells were cultured with the short-acting \u03b2<jats:sub>2<\/jats:sub>-agonist salbutamol or the long-acting \u03b2<jats:sub>2<\/jats:sub>-agonist salmeterol prior to stimulation with HDE. \u03b2<jats:sub>2<\/jats:sub>-Agonist treatment significantly increased PKA activation and significantly decreased HDE-stimulated IL-6 and IL-8 production in a concentration- and time-dependent manner. Salbutamol treatment significantly reduced HDE-induced intracellular adhesion molecule-1 expression and neutrophil adhesion to epithelial cells. Using an established intranasal inhalation exposure model, we found that salbutamol pretreatment reduced airway neutrophil influx and IL-6, TNF-\u03b1, CXCL1, and CXCL2 release in bronchoalveolar lavage fluid following a one-time exposure to HDE. Likewise, when mice were pretreated daily with salbutamol prior to HDE exposure for 3 wk, HDE-induced neutrophil influx and inflammatory mediator production were also reduced. The severity of HDE-induced lung pathology in mice repetitively exposed to HDE for 3 wk was also decreased with daily salbutamol pretreatment. Together, these results support the need for future clinical investigations to evaluate the utility of \u03b2<jats:sub>2<\/jats:sub>-agonist therapies in the treatment of airway inflammation associated with CAFO dust exposure. <\/jats:p>","DOI":"10.1152\/ajplung.00125.2016","type":"journal-article","created":{"date-parts":[[2016,5,17]],"date-time":"2016-05-17T23:49:48Z","timestamp":1463528988000},"page":"L101-L110","source":"Crossref","is-referenced-by-count":19,"title":["\u03b2<sub>2<\/sub>-Adrenergic agonists attenuate organic dust-induced lung inflammation"],"prefix":"10.1152","volume":"311","author":[{"given":"Debra J.","family":"Romberger","sequence":"first","affiliation":[{"name":"Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, Nebraska;"},{"name":"Pulmonary, Critical Care, Sleep, and Allergy Division, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Art J.","family":"Heires","sequence":"additional","affiliation":[{"name":"Pulmonary, Critical Care, Sleep, and Allergy Division, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tara M.","family":"Nordgren","sequence":"additional","affiliation":[{"name":"Pulmonary, Critical Care, Sleep, and Allergy Division, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jill A.","family":"Poole","sequence":"additional","affiliation":[{"name":"Pulmonary, Critical Care, Sleep, and Allergy Division, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Myron L.","family":"Toews","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, Nebraska;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William W.","family":"West","sequence":"additional","affiliation":[{"name":"Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska; 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