{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,27]],"date-time":"2026-03-27T13:03:09Z","timestamp":1774616589366,"version":"3.50.1"},"reference-count":42,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2001,2,1]],"date-time":"2001-02-01T00:00:00Z","timestamp":980985600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2001,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Surfactant proteins A (SP-A) and D (SP-D) are important in the innate host defense against pathogenic microorganisms. A deficit in these proteins in premature infants, either because of immaturity or as a consequence of superimposed chronic lung disease (CLD), could increase their susceptibility to infection. The study reported here examined infection in CLD in the premature newborn baboon, and correlated it with the amounts of SP-A and SP-D in lung tissue and lavage fluid. Two groups of baboons were delivered prematurely, at 125 d gestational age (g.a.), and differed principally in whether they developed naturally acquired pulmonary infections and sepsis. Group I animals were ventilated with clinically appropriate oxygen for 6 d and 14 d without clinical incident. Group II animals were ventilated for 5 to 71 d, but differed from those in Group I in that most developed pulmonary infection and\/or sepsis. In Group I animals, tissue pools of both SP-A and SP-D were equal to or exceeded those in adults, and lavage pools of SP-A increased progressively with the time of ventilation to about 35% of adult levels after 14 d. In contrast, most Group II animals had concentrations of lavage SP-A that were less than 20% of that in adult animals. A low concentration of lavage SP-A correlated with the release of interleukin-8, and with a high \u201cinfection index\u201d based on histopathology, microbiologic cultures, and clinical indications of sepsis. Our data suggest that the amounts of SP-A and SP-D in lavage fluid are indicators of the risk of infection in the evolution of neonatal CLD. Deficits in the amount of lavage SP-A, even after 60 d of ventilation, may have inhibited the resolution of infection and thereby contributed to the developing injury among our Group II animals.<\/jats:p>","DOI":"10.1164\/ajrccm.163.2.2004168","type":"journal-article","created":{"date-parts":[[2013,4,4]],"date-time":"2013-04-04T14:34:39Z","timestamp":1365086079000},"page":"389-397","source":"Crossref","is-referenced-by-count":52,"title":["Deficiencies in Lung Surfactant Proteins A and D Are Associated with Lung Infection in Very Premature Neonatal Baboons"],"prefix":"10.1093","volume":"163","author":[{"given":"SHANJANA","family":"AWASTHI","sequence":"first","affiliation":[{"name":"Departments of Physiology, Pathology, and Pediatrics, University of Texas Health Science Center, and Southwest Foundation for Biomedical Research, San Antonio, Texas; and Department of Pathology, Washington University School of Medicine, St. Louis, Missouri"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"JACQUELINE J.","family":"COALSON","sequence":"additional","affiliation":[{"name":"Departments of Physiology, Pathology, and Pediatrics, University of Texas Health Science Center, and Southwest Foundation for Biomedical Research, San Antonio, Texas; and Department of Pathology, Washington University School of Medicine, St. Louis, Missouri"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"BRADLEY A.","family":"YODER","sequence":"additional","affiliation":[{"name":"Departments of Physiology, Pathology, and Pediatrics, University of Texas Health Science Center, and Southwest Foundation for Biomedical Research, San Antonio, Texas; and Department of Pathology, Washington University School of Medicine, St. Louis, Missouri"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"ERIKA","family":"CROUCH","sequence":"additional","affiliation":[{"name":"Departments of Physiology, Pathology, and Pediatrics, University of Texas Health Science Center, and Southwest Foundation for Biomedical Research, San Antonio, Texas; and Department of Pathology, Washington University School of Medicine, St. Louis, Missouri"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"RICHARD J.","family":"KING","sequence":"additional","affiliation":[{"name":"Departments of Physiology, Pathology, and Pediatrics, University of Texas Health Science Center, and Southwest Foundation for Biomedical Research, San Antonio, Texas; and Department of Pathology, Washington University School of Medicine, St. Louis, Missouri"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2001,2,1]]},"reference":[{"key":"2026032708164569700_B1","doi-asserted-by":"crossref","first-page":"605","DOI":"10.1016\/S0022-3476(95)70362-4","article-title":"Changing trends in the epidemiology and pathogensis of neonatal chronic lung 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