Abstract
The epithelial cells of the lung are at the interface of a host and its environment and are therefore directly exposed to the inhaled air-borne particles. Rather than serving as a simple physical barrier, airway epithelia detect allergens and other irritants and then help organize the subsequent immune response through release of a plethora of secreted signals. Many of these signals are generated in response to opening of store-operated Ca2+ channels in the plasma membrane. In this review, we describe the properties of airway store-operated channels and their role in regulating airway epithelial cell function.This article is part of the themed issue ‘Evolution brings Ca2+ and ATP together to control life and death’.
Highlights
Atopic asthma is the most common chronic disease in children in the Western world, and the number of cases continues to grow
Airway epithelial cells lining the respiratory tract provide a first line of defence to air-borne pathogens and irritants, and play a central role in initiating and orchestrating subsequent innate and adaptive immune responses
In addition to these physiological functions, airway epithelial cells contribute to the remodelling process characteristic of chronic asthma
Summary
Atopic asthma is the most common chronic disease in children in the Western world, and the number of cases continues to grow. Epithelia-derived stimulants include ATP, uric acid, lysophosphatidic acid, granulocyte macrophagecolony stimulating factor, chemokine (C–C motif) ligand 2/20 (CCL2/CCL20) chemokine ligands, prostaglandin E2, thymic stromal lymphopoietin, regulated on activation, normal t expressed and secreted (RANTES) and various interleukins (ILs), including IL-1, -8 and -33 [6,7]. These signals target the components of both the innate and adaptive immune system, with important roles for antigenpresenting lung dendritic cells, mast cells and Th2 lymphocytes. As with many other cell types, it turns out that cytoplasmic Ca2þ is a critical intracellular signal in airway epithelia and this trigger Ca2þ is mainly derived from store-operated Ca2þ channels in the plasma membrane
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