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Titolo:
Anti-neutrophil chemokine preserves alveolar development in hyperoxia-exposed newborn rats
Autore:
Auten, RL; Mason, SN; Tanaka, DT; Welty-Wolf, K; Whorton, MH;
Indirizzi:
Duke Univ, Med Ctr, Neonatal Perinatal Res Inst, Dept Pediat,Div Neonatal Med, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 diat,Div Neonatal Med, Durham, NC 27710 USA Duke Univ, Med Ctr, Div Pulm & Crit Care Med, Dept Med, Durham, NC 27710 USA Duke Univ Durham NC USA 27710 it Care Med, Dept Med, Durham, NC 27710 USA Univ N Carolina, Comprehens Ctr Inflammatory Disorders, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 rders, Chapel Hill, NC 27599 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 2, volume: 281, anno: 2001,
pagine: L336 - L344
SICI:
1040-0605(200108)281:2<L336:ACPADI>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC LUNG-DISEASE; BRONCHOALVEOLAR LAVAGE FLUID; MESSENGER-RNA; BRONCHOPULMONARY DYSPLASIA; SURFACTANT PROTEIN; BRONCHIOLAR EPITHELIUM; LIPID-PEROXIDATION; ACUTE-PANCREATITIS; PREMATURE-INFANTS; PRETERM INFANTS;
Keywords:
chemotactic factors; proliferation; bromodeoxyuridine; proliferating cell nuclear antigen;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Auten, RL DUMC Box 3179, Durham, NC 27710 USA DUMC Box 3179 Durham NC USA27710 ox 3179, Durham, NC 27710 USA
Citazione:
R.L. Auten et al., "Anti-neutrophil chemokine preserves alveolar development in hyperoxia-exposed newborn rats", AM J P-LUNG, 281(2), 2001, pp. L336-L344

Abstract

Inflammation may contribute to lung injury and impaired alveolar development in bronchopulmonary dysplasia. We treated hyperoxia-exposed newborn ratswith antibodies to the neutrophil chemokine cytokine-induced neutrophil chemoattractant-1 (CINC-1) during 95% O-2 exposure to reduce adverse effects of hyperoxia-induced inflammation on lung development. Rats were exposed atbirth to air, 95% O-2, or 95% O-2 + anti-CINC-1 (injected on days 3 and 4). Bromodeoxyuridine (BrdU) was injected 6 h before death. Anti-CINC-1 treatment improved weight gain but not survival at day 8. Anti-CINC-1 reduced bronchoalveolar lavage neutrophils at day 8 to levels equal to air controls. Total detectable lung CINC-1 was reduced to air control levels. Lung compliance was improved by anti-CINC-1, achieving air control levels in the 10-mganti-CINC-1 group. Anti-CINC-1 preserved proliferating cell nuclear antigen expression in airway epithelium despite 95% O-2 exposure. BrdU incorporation was depressed by hyperoxia but preserved by anti-CINC-1 to levels similar to air control. Alveolar volume and surface density were decreased by hyperoxia but preserved by anti-CINC-1 to levels equal to air control. Blockade of neutrophil influx in newborns may avert early lung injury and avoid alveolar developmental arrest that contributes to bronchopulmonary dysplasia.

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Documento generato il 20/01/21 alle ore 02:09:33