{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,4,17]],"date-time":"2024-04-17T07:43:45Z","timestamp":1713339825341},"reference-count":44,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2003,4,3]],"date-time":"2003-04-03T00:00:00Z","timestamp":1049328000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pediatric Pulmonology"],"published-print":{"date-parts":[[2003,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The first objective of this study was to evaluate longitudinal changes in respiratory burst activity in circulating neutrophils and monocytes in infants of less than 30 weeks of gestation with respiratory distress syndrome (RDS), and to examine differences in neonates who subsequently developed bronchopulmonary dysplasia (BPD) compared with those neonates who did not. The second objective was to investigate the effects of dexamethasone on respiratory burst activity in neutrophils and monocytes. We measured burst activity on neutrophils and monocytes in fresh heparinized blood in response to <jats:italic>E. coli<\/jats:italic>, N\u2010formyl\u2010met\u2010leu\u2010phe (fMLP), and phorbol 12\u2010myristate 13\u2010acetate stimulation on days 3, 7, 14, and 21 of life, before and 2\u20133 days after initiating a 6\u2010day course of dexamethasone treatment. Infants with RDS participating in the study were followed until discharge, and were classified as non\u2010BPD and either 1) BPD d28, reflecting their oxygen requirement at day of life 28, or 2) BPD 36 weeks, reflecting oxygen dependence at 36 weeks' corrected gestational age. The diagnosis of BPD was supported by radiological changes of BPD. The percentage of activated neutrophils producing a respiratory burst increased in all premature infants with increasing postnatal days during the first 28 days of life, when the physiological stimulus <jats:italic>E. coli<\/jats:italic> was used as an activator (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.02). There was no significant difference in respiratory burst activity measured either as percent activation or as mean fluorescence intensity between non\u2010BPD and BPD infants after adjusting for the difference in weight and gestational age between the two groups. The treatment of premature infants with dexamethasone was associated with decreased activation of neutrophils (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.005) when <jats:italic>E. coli<\/jats:italic> was used as a stimulus. In conclusion, a significant increase in neutrophil respiratory burst activity occurs during the first month of life in very low birth weight infants. Greater pulmonary damage in BPD cannot be attributed to reduced burst activity in either neutrophils or monocytes. Dexamethasone treatment was associated with decreased neutrophil respiratory burst activity. Pediatr Pulmonol. 2003; 35:392\u2013399. \u00a9 2003 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ppul.10279","type":"journal-article","created":{"date-parts":[[2003,4,7]],"date-time":"2003-04-07T15:03:25Z","timestamp":1049727805000},"page":"392-399","source":"Crossref","is-referenced-by-count":8,"title":["Respiratory burst activity in bronchopulmonary dysplasia and changes with 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