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Crosstalk Between Alveolar Epithelial Cells and Macrophages in Asthma

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Genomic Approach to Asthma

Part of the book series: Translational Bioinformatics ((TRBIO,volume 12))

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Abstract

Patients with allergic asthma is characterized by activation and infiltration of eosinophils and Th2 lymphocytes. However, patients with atopic severe asthma have predomiant pulmonary infiltrates of neutrophils and Th17 lymphocytes and are insensitive to the treatment of long-acting beta adrenoceptor agonist (LABA) and glucocorticoids. Airway epithelilial cells and macrophages orchestrate the hypersensitive reaction through both cell contact and release of variable pro- and anti-inflammatory cytokines, chemokines and other mediators. The activated type I epithelial cells produce and release variable allergic mediators, such as TSLP (thymic stromal lymphopoietin), IL-33 and IL-25, etc. after exposure to allegens. Type II epithelial cells constitutively produce surfactant proteins A and D, participate in phagocytosis of invading pathogens and moduate innate immnity of alveolar macrophages. IL-33 up-regulates IL-13 release from activated alveolar macrophages and type 2 innate lymphoid cells (ILC2) cells through membrane-bound ST2 (IL-33 receptor) signal. The released IL-13 promotes mucus production, lung fibrosis and polarization of alternatively alveolar macrophages (M2 macrophages). This chapter outlines existing knowledge on the role and interactin of alveolar epithelial cells and macrophages in allergic airway inflammation, and discusses the potential applicatin of the cells in the immunotherapy of asthma.

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Jiang, Z. (2018). Crosstalk Between Alveolar Epithelial Cells and Macrophages in Asthma. In: Wang, X., Chen, Z. (eds) Genomic Approach to Asthma. Translational Bioinformatics, vol 12. Springer, Singapore. https://doi.org/10.1007/978-981-10-8764-6_11

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