ArticleRespiratory research2026
Aryl hydrocarbon receptor (AhR) regulates organic dust and organic dust-associated bacterial extracellular vesicles-induced airway inflammation via ROS-dependent NFκB and STAT3 activation.
Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundExposure to agricultural organic dust increases the risk of respiratory diseases. Aryl hydrocarbon receptor (AhR), a transcription factor activated by environmental chemicals and endogenous metabolites, regulates immune and inflammatory responses, but its role in organic dust-induced lung inflammation is not known. Our study elucidated mechanisms by which AhR modulates bronchial epithelial cell inflammatory responses induced by poultry farm organic dust extract (DE) and organic dust-associated (OD) bacterial extracellular vesicles (EVs).
methodsThe role of AhR in the DE- and OD-bacterial EVs-mediated inflammatory responses in Beas2B bronchial epithelial cells was investigated using siRNA knockdown. AhR expression and nuclear translocation, reactive oxygen species (ROS), and inflammatory mediator (pro-IL-1β, ICAM-1, IL-6, IL-8) levels were evaluated by western immunoblotting, immunostaining, DCFDA labeling, real-time qRT-PCR, and ELISA. The induction of lung inflammatory cytokines by OD-bacterial EVs was assessed by ELISA in AhR knockout mice.
resultsDE and OD-bacterial EVs increased AhR protein expression and nuclear translocation in a time-dependent manner in Beas2B cells. AhR knockdown reduced ROS and NFκB activation but modulated STAT3 differentially, suppressing DE-induced activation while enhancing OD-bacterial EV-induced activation. Nevertheless, AhR knockdown attenuated the induction of inflammatory mediators by DE and OD-bacterial EVs. Inhibition of NOX, XO, NFκB, and STAT3 attenuated AhR increase by DE- and OD-bacterial EVs. Studies in AhR knockout mice demonstrated that AhR regulates lung inflammatory cytokines in a sex-specific manner.
conclusionAhR is a critical modulator of organic dust-induced lung inflammation, potentially driven by a positive feedback loop involving ROS and NFκB/STAT3. Targeting the AhR pathway offers a therapeutic strategy for respiratory diseases afflicting agricultural workers.
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