Journal
RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY
Volume 178, Issue 3, Pages 449-457Publisher
ELSEVIER
DOI: 10.1016/j.resp.2011.06.026
Keywords
Brainstem; Inflammation; Hypoxia; Neonatal apnea; Prostaglandin; Dysautonomia
Categories
Funding
- Swedish Research Council
- Stockholm County Council
- Karolinska Institutet
- M & M Wallenberg Foundation
- Swedish National Heart and Lung Foundation
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Infection in infancy may dramatically aggravate an underlying cardiorespiratory dysfunction during a susceptible postnatal period. Children with immature brainstem respiratory control, as well as infants, may have periodic irregular breathing with potential detrimental apneas that are increased during sleep as well as during infectious episodes. Data now indicate that the proinflammatory cytokine interleukin (IL)-1 beta impairs respiration during infection via prostaglandin E2 (PGE(2)) and that infection, with associated eicosanoid release, is one of the main causes of respiratory disorders in preterm infants. Moreover, brainstem microsomal prostaglandin E synthase-1 (mPGES-1) is rapidly activated during transient hypoxia. An inflammatory mediated activation of the mPGES-1 pathway, e.g., by viral or bacterial infection, rapidly induces release of PGE2 in the vicinity of brainstem cardio-respiratory-related centers. This will depress the autonomic control networks, including the central drive to breathe. Hypoxia may then further reduce the activity of vital brainstem centers and the ability to autoresuscitate. This might have fatal consequences in vulnerable infants during a susceptible time frame. Here the evidence from human, animal and molecular studies to support this hypothesis is reviewed and how the pathogenesis of apnea and the response to hypoxia is associated with inflammatory pathways is discussed. (C) 2011 Elsevier B.V. All rights reserved.
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