Inflammatory mechanisms linking maternal and childhood asthma. Issue 1 (10th February 2020)

• Record Type: Journal Article
• Authors: Lebold, Katie M.; Jacoby, David B.; Drake, Matthew G.
• Is Part Of: Journal of leukocyte biology. Volume 108:Issue 1(2020)
• Page Start: 113
• Page End: 121
• Publication Date: 2020-02-10
• Subjects: asthma -- childhood -- developmental origins -- eosinophil -- inflammation -- maternal -- nerves; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1002/JLB.3MR1219-338R
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract: Asthma is a chronic inflammatory airway disease characterized by airway hyperresponsiveness, inflammation, and remodeling. Asthma often develops during childhood and causes lifelong decrements in lung function and quality of life. Risk factors for childhood asthma are numerous and include genetic, epigenetic, developmental, and environmental factors. Uncontrolled maternal asthma during pregnancy exposes the developing fetus to inflammatory insults, which further increase the risk of childhood asthma independent of genetic predisposition. This review focuses on the role of maternal asthma in the development of asthma in offspring. We will present maternal asthma as a targetable and modifiable risk factor for childhood asthma and discuss the mechanisms by which maternal inflammation increases childhood asthma risk. Topics include how exposure to maternal asthma in utero shapes structural lung development with a special emphasis on airway nerves, how maternal type‐2 cytokines such as IL‐5 activate the fetal immune system, and how changes in lung and immune cell development inform responses to aero‐allergens later in life. Finally, we highlight emerging evidence that maternal asthma establishes a unique "asthma signature" in the airways of children, leading to novel mechanisms of airway hyperreactivity and inflammatory cell responses. Abstract : Review on the impact of maternal asthma on fetal development, with an emphasis on how maternal cytokines contribute to increased asthma risk in offspring .