{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T22:07:10Z","timestamp":1786486030230,"version":"build-2736575974"},"reference-count":46,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2025,10,14]],"date-time":"2025-10-14T00:00:00Z","timestamp":1760400000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,10,14]],"date-time":"2025-10-14T00:00:00Z","timestamp":1760400000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI141372"],"award-info":[{"award-number":["AI141372"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002570","name":"American Association of Immunologists","doi-asserted-by":"publisher","award":["AAI"],"award-info":[{"award-number":["AAI"]}],"id":[{"id":"10.13039\/100002570","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["AI168603"],"award-info":[{"award-number":["AI168603"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2025,10,14]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Type I interferons (IFNs) play complex roles during bacterial infections. We previously found that type I IFNs were induced in\n                      <jats:italic toggle=\"yes\">Bordetella pertussis<\/jats:italic>\n                      -infected adult mice but not in infant mice, a potentially relevant clinical dichotomy, since pertussis can be fatal in human infants. We investigated the role of type I IFNs and their cross-regulation with type III IFNs (IFN-\u03bb) in\n                      <jats:italic toggle=\"yes\">B. pertussis<\/jats:italic>\n                      infection across developmental stages. In contrast to global IFNAR1 knockout adult mice, in which lung inflammation was equivalent to that in wild-type mice, myeloid cell-specific deficiency of the type I IFN receptor protein IFNAR1 (LysM\n                      <jats:sup>Cre<\/jats:sup>\n                      IFNAR1\n                      <jats:sup>fl\/fl<\/jats:sup>\n                      ) resulted in significantly reduced lung inflammation and pro-inflammatory cytokine production, despite elevated pulmonary IFN-\u03bb levels. Mechanistically, we found that, in contrast to WT macrophages, IFNAR1-deficient macrophages produced IFN-\u03bb in response to\n                      <jats:italic toggle=\"yes\">B. pertussis<\/jats:italic>\n                      or pertussis toxin, a process dependent on the G protein-coupled receptor lysophosphatidic acid receptor 1 (LPAR1). IFNAR1 deficiency did not affect type I IFN expression or killing capacity by macrophages and neutrophils. In striking contrast to WT infant mice, which developed resistance to lethal\n                      <jats:italic toggle=\"yes\">B. pertussis<\/jats:italic>\n                      infection by postnatal day 10 (P10), LysM\n                      <jats:sup>Cre<\/jats:sup>\n                      IFNAR1\n                      <jats:sup>fl\/fl<\/jats:sup>\n                      infant mice remained highly susceptible to lethal infection through P21, exhibiting increased lung bacterial burden and inflammation, as well as increased bacterial dissemination compared to WT infant mice. These findings reveal a critical age- and cell-specific interplay between type I and III IFNs during\n                      <jats:italic toggle=\"yes\">B. pertussis<\/jats:italic>\n                      infection and highlight a novel LPAR1-dependent pathway for IFN-\u03bb induction in the absence of type I IFN signaling.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00306-25","type":"journal-article","created":{"date-parts":[[2025,9,22]],"date-time":"2025-09-22T12:00:54Z","timestamp":1758542454000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":4,"title":["Myeloid cell-specific type I interferon signaling mediates age-dependent inflammation and protection in\n                    <i>Bordetella pertussis<\/i>\n                    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