Queensland Children's Medical Research Institute, University of Queensland, Brisbane, Queensland, Australia.
Curr Opin Allergy Clin Immunol. 2011 Apr;11(2):127-31. doi: 10.1097/ACI.0b013e32834487c6.
Asthma is essentially a developmental disease, in which the normal growth and development of the respiratory and immune systems are affected by environmental exposures acting on underlying genetic predispositions. The purpose of this review is to examine the role of innate immunity in the lungs in the development of allergy and asthma.
Both the innate and adaptive arms of the immune system are immature at birth and undergo prolonged periods of postnatal maturation. As such, they are vulnerable to adverse environmental exposures, both before and after birth. Both genetic predispositions and environmentally induced epigenetic changes in gene expression are likely to contribute to the risk of asthma; however, the relative contributions are unclear. Increasing interest is focused on deficient innate responses of the respiratory epithelium to viral infections and how these may increase the risk of asthma. However, definitive proof that these are primary and not secondary effects is lacking. Although most research has concentrated on the role of respiratory viral infections in increasing the asthma risk, the recent suggestion that the lung has a resident bacteriome and potentially important viral-bacterial interactions in the lungs broadens research scope in this area.
Classic risk factors for asthma include a family history of asthma and allergies, early and persistent allergic sensitization and viral lower-respiratory infections in early life. However, these factors do not fully explain the risk. Perhaps, the resident pulmonary microbiome and the immune response that this generates during respiratory viral infections will provide the 'missing link' in the epidemiology.
哮喘本质上是一种发育性疾病，其呼吸系统和免疫系统的正常生长和发育受到遗传易感性基础上的环境暴露的影响。本文的目的在于探讨肺部固有免疫在过敏和哮喘发生中的作用。
免疫系统的固有免疫和适应性免疫在出生时均不成熟，并在出生后经历长时间的成熟过程。因此，它们易受到出生前后的不利环境暴露的影响。遗传易感性和环境诱导的基因表达表观遗传变化都可能导致哮喘的风险增加；然而，相对贡献尚不清楚。越来越多的研究关注呼吸道上皮对病毒感染的固有反应不足以及如何增加哮喘风险，但缺乏明确的证据表明这些是原发性而非继发性效应。虽然大多数研究都集中在呼吸道病毒感染增加哮喘风险的作用上，但最近有研究表明，肺部存在常驻菌丛，以及肺部潜在的重要病毒-细菌相互作用，这拓宽了该领域的研究范围。
哮喘的经典危险因素包括哮喘和过敏家族史、早期和持续的过敏致敏以及生命早期的呼吸道病毒感染。然而，这些因素并不能完全解释风险。也许，肺部常驻微生物群及其在呼吸道病毒感染过程中产生的免疫反应将为流行病学提供“缺失的一环”。
