Effects of heat shock and hypoxia on neonatal neutrophil lipopolysaccharide responses: altered apoptosis, Toll-like receptor-4 and CD11b expression compared with adults
| Autor: | Cormac T. Taylor, Margaret Sheridan-Pereira, Julie J Grantham, John M. Fitzpatrick, R. William G. Watson, Eleanor J. Molloy, Belinda T. Doyle, Amanda O'Neill, David Webb |
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| Rok vydání: | 2005 |
| Předmět: |
Adult
Lipopolysaccharides Male medicine.medical_specialty Aging Hot Temperature Lipopolysaccharide Neutrophils Apoptosis Gestational Age macromolecular substances Cd11b expression chemistry.chemical_compound Internal medicine medicine Humans Toll-like receptor CD11b Antigen biology business.industry Infant Newborn Cell hypoxia Hypoxia (medical) Fetal Blood Cell Hypoxia Toll-Like Receptor 4 Endocrinology Integrin alpha M chemistry Pediatrics Perinatology and Child Health Immunology biology.protein Female medicine.symptom business Developmental Biology |
| Zdroj: | Biology of the neonate. 90(1) |
| ISSN: | 0006-3126 |
| Popis: | Background: Dysfunctional inflammatory responses have been implicated in several neonatal inflammatory disorders following infection and hypoxia. Objectives: We aimed to study the effects of in vitro hypoxia and heat shock (HS) on normal adult and newborn neutrophil migration (CD11b) and persistence (apoptosis) following lipopolysaccharide (LPS) stimulation. Methods: The mechanism for altered LPS responses was assessed at the level of the LPS signalling receptors, Toll-like receptor-4 (TLR-4), TLR-2 and CD14 expression in normal neonates and adults. Results: In adults, although hypoxia delayed neutrophil apoptosis, LPS enhanced this response. In contrast, HS (42°C) increased adult apoptotic rates and abrogated the LPS responses. Both hypoxia and HS prevented the LPS-induced increase in adult CD11b although it was unaltered in neonates. Adult TLR-4 neutrophil expression was increased by LPS and hypoxia, and decreased in HS, possibly explaining their variable LPS responsiveness. In contrast, neonatal neutrophils were LPS hyporesponsive which may be mediated by failure of TLR-4 upregulation with LPS. Conclusions: Neonates do not have increased LPS responsiveness in hypoxia or heat shock in vitro, which may prevent hyperinflammation and thereby minimise tissue damage in inflammation or infection. |
| Databáze: | OpenAIRE |
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