The Role of Mast Cells in Aspirin-Exacerbated Respiratory Disease (AERD) Pathogenesis: Implications for Future Therapeutics.
Merin Elizabeth KuruvillaKristine VanijcharoenkarnJoshua M LevyPublished in: Journal of asthma and allergy (2020)
Mast cells (MC) have recently been demonstrated to play an integral role in the pathogenesis of aspirin-exacerbated respiratory disease (AERD). When activated, MCs release pre-formed granules of many pro-inflammatory mediators, including histamine, serotonin, and various chemokines and cytokines including tumor necrosis factor (TNF)-α, interferon ɣ (IFN ɣ), macrophage inhibitory factor, transforming growth factor, interleukin (IL) 1, 3-6, 9, 10, 13 and 16. These mediators promote inflammation in AERD by recruiting or activating a network of cells involved in acute and chronic inflammatory pathways, such as endothelial, epithelial, stromal, and other immune cells. Several studies have implicated multifactorial pathways for MC activation in AERD beyond classical IgE mediated mechanisms. The elucidation of these complex networks therefore represents important targets for innovative patient therapeutics. This review summarizes classic and alternative pathways of MC activation in AERD with a special focus in relation to new and emerging treatment strategies.
Keyphrases
- transforming growth factor
- low dose
- oxidative stress
- rheumatoid arthritis
- epithelial mesenchymal transition
- induced apoptosis
- dendritic cells
- small molecule
- cardiovascular events
- antiplatelet therapy
- signaling pathway
- immune response
- adipose tissue
- drug induced
- case report
- bone marrow
- type diabetes
- respiratory failure
- cell proliferation
- intensive care unit
- aortic dissection
- percutaneous coronary intervention
- atrial fibrillation
- anti inflammatory drugs
- case control