Neonatal Research Unit, Q2:07, Department of Women's and Children's Health, Astrid Lindgren Children's Hospital, Karolinska Institutet, Karolinska University Hospital at Solna, S-171 76 Stockholm, Sweden.
Respir Physiol Neurobiol. 2011 Sep 30;178(3):449-57. doi: 10.1016/j.resp.2011.06.026. Epub 2011 Jul 6.
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)-1β 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 PGE(2) 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.
婴儿时期的感染可能会在易感的产后期间显著加重潜在的心肺功能障碍。不成熟的脑干呼吸控制的儿童以及婴儿可能会出现周期性的不规则呼吸，潜在的有害呼吸暂停会增加，无论是在睡眠期间还是在感染期间。现在的数据表明，促炎细胞因子白细胞介素 (IL)-1β 通过前列腺素 E2 (PGE2) 在感染期间损害呼吸，并且感染与相关的类花生酸释放是早产儿呼吸障碍的主要原因之一。此外，脑干微粒体前列腺素 E 合酶-1 (mPGES-1) 在短暂缺氧期间迅速激活。炎症介导的 mPGES-1 途径的激活，例如病毒或细菌感染，会迅速在脑干与心肺相关中心附近释放 PGE2。这将抑制自主控制网络，包括呼吸的中枢驱动。缺氧随后可能进一步降低重要脑干中心的活性和自主复苏的能力。在易受伤害的时期，这可能对脆弱的婴儿产生致命的后果。在这里，回顾了来自人类、动物和分子研究的证据来支持这一假设，以及呼吸暂停的发病机制和对缺氧的反应如何与炎症途径相关。
