{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T01:37:32Z","timestamp":1790905052744,"version":"4.1.0"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2024,1,29]],"date-time":"2024-01-29T00:00:00Z","timestamp":1706486400000},"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":["AI141372"],"award-info":[{"award-number":["AI141372"]}],"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":["AI156042"],"award-info":[{"award-number":["AI156042"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008510","name":"University of Maryland","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008510","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Baltimore Institute for Clinical and Translational Research grant"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,5,29]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Many respiratory infections are selectively injurious to infants, yet the etiology of age-associated susceptibility is unknown. One such bacterial pathogen is Bordetella pertussis. In adult mice, innate interferon \u03b3 (IFN-\u03b3) is produced by natural killer (NK) cells and restricts infection to the respiratory tract. In contrast, infant pertussis resembles disease in NK cell\u2013 and IFN-\u03b3\u2013deficient adult mice that experience disseminated lethal infection. We hypothesized that infants exhibit age-associated deficits in NK cell frequency, maturation, and responsiveness to B. pertussis, associated with low IFN-\u03b3 levels. To delineate mechanisms behind age-dependent susceptibility, we compared infant and adult mouse models of infection. Infection in infant mice resulted in impaired upregulation of IFN-\u03b3 and substantial bacterial dissemination. B. pertussis\u2013infected infant mice displayed fewer pulmonary NK cells than adult mice. Furthermore, the NK cells in the infant mouse lungs had an immature phenotype, and the infant lung showed no upregulation of the IFN-\u03b3\u2013inducing cytokine IL-12p70. Adoptive transfer of adult NK cells into infants, or treatment with exogenous IFN-\u03b3, significantly reduced bacterial dissemination. These data indicate that the lack of NK cell\u2013produced IFN-\u03b3 significantly contributes to infant fulminant pertussis and could be the basis for other pathogen-induced, age-dependent respiratory diseases.<\/jats:p>","DOI":"10.1093\/jleuko\/qiae020","type":"journal-article","created":{"date-parts":[[2024,1,29]],"date-time":"2024-01-29T19:26:00Z","timestamp":1706556360000},"page":"1143-1153","source":"Crossref","is-referenced-by-count":11,"title":["Age-dependent natural killer cell and interferon \u03b3 deficits contribute to severe pertussis in infant mice"],"prefix":"10.1093","volume":"115","author":[{"given":"Ashley E","family":"Mitchell","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 W. Baltimore St., Baltimore, MD 21201 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen M","family":"Scanlon","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 W. Baltimore St., Baltimore, MD 21201 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily M","family":"Flowers","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 W. Baltimore St., Baltimore, MD 21201 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cassandra M","family":"Jordan","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 W. Baltimore St., Baltimore, MD 21201 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellis J","family":"Tibbs","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 W. Baltimore St., Baltimore, MD 21201 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alicia","family":"Bukowski","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 W. Baltimore St., Baltimore, MD 21201 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Danisha","family":"Gallop","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 W. Baltimore St., Baltimore, MD 21201 , United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas H","family":"Carbonetti","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , 685 W. 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