{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T14:06:26Z","timestamp":1787580386407,"version":"build-2736575974"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T00:00:00Z","timestamp":1771891200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["1R01HL154549"],"award-info":[{"award-number":["1R01HL154549"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R21AI156597"],"award-info":[{"award-number":["R21AI156597"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001680","name":"Charles Hood Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001680","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100018130","name":"Department of Pediatrics","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100018130","id-type":"DOI","asserted-by":"publisher"}]},{"name":"MGH for Lung Cell Bank"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,6,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Airflow obstruction unresponsive to \u03b22 adrenergic receptor (\u03b22AR) agonists is a key feature of infant respiratory syncytial virus (RSV) bronchiolitis. The underlying mechanisms remain poorly understood, and effective treatment is lacking.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To investigate whether and how infant RSV infection affects \u03b22AR signaling in airway smooth muscle cells (ASMCs).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We established complementary human and mouse models of RSV infection using infant (0-18\u2009months) precision-cut lung slices (PCLSs), neonatal epithelial air-liquid interface (ALI) culture, and mouse pups to assess \u03b22AR-mediated ASMC relaxation. Cytokine profiling was performed using conditioned medium (CM) from RSV-infected neonatal ALI culture. Infant ASMCs treated with CM were subjected to bulk RNA sequencing and \u03b22AR expression and function assays. Findings were validated with nasopharyngeal aspirates (NPAs) from infants with severe bronchiolitis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and main results<\/jats:title>\n                    <jats:p>RSV selectively targeted infant bronchial epithelium, inducing cytokine secretion that impaired \u03b22AR-mediated ASMC relaxation. CXCL11 was the most upregulated epithelial cytokine and signaled to infant ASMCs through ACKR3, a \u03b2-arrestin\u2013poised receptor that interacted with \u03b22AR to promote its phosphorylation, internalization, and degradation. Using mouse strains with genetic variation in Cxcl11, along with ACKR3 blockade and CXCL11 rescue assays, we demonstrated that CXCL11-ACKR3 signaling was both necessary and sufficient for \u03b22AR dysfunction. Moreover, blockade of CXCL11 or ACKR3 restored \u03b22AR responsiveness in infant PCLSs exposed to RSV or NPA from severe RSV bronchiolitis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Infant RSV bronchiolitis exploits CXCL11-ACKR3 signaling to desensitize \u03b22AR in ASMCs. Targeting this pathway may improve \u03b22AR agonist efficacy in severe RSV bronchiolitis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/ajrccm\/aamag087","type":"journal-article","created":{"date-parts":[[2026,2,18]],"date-time":"2026-02-18T12:41:44Z","timestamp":1771418504000},"page":"1290-1304","source":"Crossref","is-referenced-by-count":2,"title":["Infant respiratory syncytial virus infection disrupts \u03b22 adrenergic airway relaxation via epithelial CXCL11"],"prefix":"10.1093","volume":"212","author":[{"given":"Caiqi","family":"Zhao","sequence":"first","affiliation":[{"name":"Division of Newborn Medicine, Department of Pediatrics, Massachusetts General Hospital , Boston, MA,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alice E","family":"Taliento","sequence":"additional","affiliation":[{"name":"Division of Newborn Medicine, Department of Pediatrics, Massachusetts General Hospital , Boston, MA,","place":["United 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