期刊
PEDIATRIC RESEARCH
卷 64, 期 4, 页码 393-398出版社
NATURE PUBLISHING GROUP
DOI: 10.1203/PDR.0b013e318180e4af
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资金
- National Institutes of Health [HD042036, GM034310, ES004738, FS005022, HL067708, CA100994, AR055073]
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [K08HD042036] Funding Source: NIH RePORTER
- NATIONAL CANCER INSTITUTE [R01CA100994] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [K01HL067708] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [U54AR055073] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES005022, R01ES004738] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM034310] Funding Source: NIH RePORTER
Lipoxin A4 is an eicosanoid that plays a key role in the resolution of neutrophilic inflammation. In these studies, we investigated the hypothesis that responses to lipoxin A4 are impaired in neonates, relative to adults. Lipoxin A4 was found to inhibit chemotaxis and respiratory burst in adult neutrophils. In contrast, it had no effect on these activities in neonatal neutrophils. In addition, while lipoxin A4 augmented apoptosis in LPS-treated adult neutrophils, apoptosis ill neonatal cells was not affected by lipoxin A4 alone or in combination with LPS. The biologic actions of anti-inflammatory eicosanoids are mediated, in part, via the transcription factor peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Expression of PPAR-gamma mRNA and its target gene, neutrophil gelatinase-associated lipocalin (NGAL). were significantly reduced in neonatal cells when compared With adult Cells. Moreover, whereas treatment of adult neUtrophils with lipoxin A4 increased PPAR-gamma expression, no effects were observed ill neonatal cells. 5- and 15-lipoxygenase, enzymes required for the synthesis of lipoxin A4, were also reduced in neonatal neutrophils. These findings suggest that the anti-inflammatory activity of lipoxin A4 is impaired in neonatal neutrophils and that this is due, in part, to reduced PPAR-gamma signaling. This may contribute to diseases associated with chronic inflammation in neonates.
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