Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6155807 | Translational Research | 2016 | 38 Pages |
Abstract
Mast cells and their activation contribute to lung health via innate and adaptive immune responses to respiratory pathogens. They are also involved in the normal response to tissue injury. However, mast cells are involved in disease processes characterized by inflammation and remodeling of tissue structure. In these diseases mast cells are often inappropriately and chronically activated. There is evidence for activation of mast cells contributing to the pathophysiology of asthma, pulmonary fibrosis, and pulmonary hypertension. They may also play a role in chronic obstructive pulmonary disease, acute respiratory distress syndrome, and lung cancer. The diverse mechanisms through which mast cells sense and interact with the external and internal microenvironment account for their role in these diseases. Newly discovered mechanisms of redistribution and interaction between mast cells, airway structural cells, and other inflammatory cells may offer novel therapeutic targets in these disease processes.
Keywords
FiO2ASMBALIP3inositol triphosphateECMITIMPaO2ARDSSCFIPAHMCTCRTKFcεRIMCASCarboxypeptidase ACADM1dihydronicotinamide-adenine dinucleotide phosphateFEV1CPAPAHTGF-β1IgEAHRNADPHMCTROSimmunoreceptor tyrosine-based inhibition motif IgE, immunoglobulin EinterferonIFNinterleukinChronic obstructive pulmonary diseaseCOPDtransforming growth factor beta 1tumor necrosis factor αRTK, Receptor tyrosine kinaseforced expiratory volume in one secondAcute respiratory distress syndromeMonoclonal mast cell activation syndromePlatelet activating factorAirway smooth muscleVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)Stem Cell FactorTNF-αpartial pressure of arterial oxygenPulmonary arterial hypertensionbronchoalveolar lavageLeukotrieneExtracellular matrixCell adhesion molecule 1PAFAirway hyperresponsivenessIdiopathic pulmonary arterial hypertensionprostaglandinReactive oxygen speciesHigh affinity IgE receptor
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Authors
Harvinder Virk, Greer Arthur, Peter Bradding,