{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T04:26:50Z","timestamp":1780547210538,"version":"3.54.1"},"reference-count":47,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,10,21]],"date-time":"2021-10-21T00:00:00Z","timestamp":1634774400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Physiol."],"abstract":"<jats:p>The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates the metabolism of xenobiotics. There is growing evidence that the AhR is implicated in physiological processes such proliferation, differentiation, and immune responses. Recently, a role of the AhR in regulating allergic asthma has been suggested, but whether the AhR also regulates other type of asthma, particularly occupational\/irritant-induced asthma, remains unknown. Using AhR-deficient (<jats:italic>Ahr<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic>) mice, we compared the function of the AhR in the response to ovalbumin (OVA; allergic asthma) vs. chlorine (Cl<jats:sub>2<\/jats:sub>; irritant-induced asthma) exposure. Lung inflammation and airway hyperresponsiveness were assessed 24h after exposure to Cl<jats:sub>2<\/jats:sub> or OVA challenge in <jats:italic>Ahr<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> and heterozygous (<jats:italic>Ahr<jats:sup>+\/\u2212<\/jats:sup><\/jats:italic>) mice. After OVA challenge, absence of AhR was associated with significantly enhanced eosinophilia and lymphocyte influx into the airways of <jats:italic>Ahr<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic> mice. There were also increased levels of interleukin-4 (IL-4) and IL-5 in the airways. However, OVA-induced airway hyperresponsiveness was not affected. In the irritant-induced asthma model caused by exposure to Cl<jats:sub>2<\/jats:sub>, the AhR did not regulate the inflammatory response. However, absence of AhR reduced Cl<jats:sub>2<\/jats:sub>-induced airway hyperresponsiveness. Collectively, these results support a differential role for the AhR in regulating asthma outcomes in response to diverse etiological agents.<\/jats:p>","DOI":"10.3389\/fphys.2021.720196","type":"journal-article","created":{"date-parts":[[2021,10,21]],"date-time":"2021-10-21T06:56:26Z","timestamp":1634799386000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":10,"title":["Differential Regulation of the Asthmatic Phenotype by the Aryl Hydrocarbon Receptor"],"prefix":"10.3389","volume":"12","author":[{"given":"Hussein","family":"Traboulsi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angela Rico","family":"de Souza","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benoit","family":"Allard","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zahraa","family":"Haidar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Sorin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vanessa","family":"Moarbes","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth D.","family":"Fixman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G.","family":"Martin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David H.","family":"Eidelman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carolyn J.","family":"Baglole","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,10,21]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","first-page":"267","DOI":"10.1111\/all.12776","article-title":"Phenotypic plasticity and targeting of Siglec-F(high) CD11c(low) eosinophils to the airway in a murine model of asthma","volume":"71","author":"Abdala Valencia","year":"2016","journal-title":"Allergy"},{"key":"ref2","doi-asserted-by":"publisher","first-page":"945","DOI":"10.1016\/j.jaci.2019.07.015","article-title":"Tolerogenic signaling of alveolar macrophages induces lung adaptation to oxidative injury","volume":"144","author":"Allard","year":"2019","journal-title":"J. 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