Explores how beta-agonists affect cytokine production in airway epithelium, implying diverse impacts on lung inflammation.
BACKGROUND: AR regulation of allergic lung inflammation remain unestablished. METHODS: To explore the potential contribution of airway epithelia in this phenomenon, we compared the ability of ractopamine (RP), recently identified as a Gs-biased beta-agonist, to that of the unbiased/balanced beta-agonist albuterol (ALB), on IL-13-stimulated mucin and cytokine production in human airway epithelia cultures in air-liquid interface (HAE). RESULTS: AR agonism for IL-13 to stimulate cytokine production, such a requirement was observed only in minority of the (12) cultures examined. CONCLUSIONS: AR agonism in vivo. Moreover, they suggest that beta-agonist effects on the cytokine profile in the allergen-inflamed lung may be influenced by specific asthmatic endotypes and involve cooperativity among multiple cell types.
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Graumuller et al. (2026) studied this question.
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