Abstract
Purpose of the Review
The connections between allergy, asthma and metabolic syndrome are becoming increasingly clear. Recent research suggests a unifying mitochondrial link between the diverse phenotypes of these interlinked morbidities. The scope of this review is to highlight cellular mechanisms, epidemiology and environmental allergens influencing mitochondrial function and its importance in allergy and asthma. We briefly also consider the potential of mitochondria-targeted therapies in prevention and cure.
Recent Findings
Recent research has shown allergy, asthma and metabolic syndrome to be linked to mitochondrial dysfunction. Environmental pollutants and allergens are observed to cause mitochondrial dysfunction, primarily by inducing oxidative stress and ROS production. Malfunctioning mitochondria change the bioenergetics of the cell and its metabolic profile to favour systemic inflammation, which drives all three types of morbidities.
Summary
Given the existing experimental evidence, approaches targeting mitochondria (e.g. antioxidant therapy and mitochondrial replacement) are being conducted in relevant disease models—with some progressing towards clinical trials, making mitochondrial function the focus of translational therapy research in asthma, allergy and linked metabolic syndrome.
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Abbreviations
- AIM2 :
-
Absent in melanoma 2
- BAL :
-
Bronchoalveolar lavage
- DrpI :
-
Dynamin 1 like protein
- ETC :
-
Electron transport chain
- IFN :
-
Interferon Gamma
- IgE :
-
Immunoglobulin E
- IL :
-
Interleukin
- KDa :
-
Kilodalton
- NLRP3 :
-
Nod Like receptor family pyrin domain containing 3
- OpaI :
-
Optic Atrophy 1
- PGC 1α :
-
Peroxisome proliferator-activated receptor gamma coactivator 1 alpha
- ROS :
-
Reactive oxygen species
- TET :
-
Ten-eleven translocation
- TFAM :
-
Transcription Factor A Mitochondrial
- Th2 :
-
T helper cells type 2
- TNFα :
-
Tumour Necrosis Factor Alpha
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Iyer, D., Mishra, N. & Agrawal, A. Mitochondrial Function in Allergic Disease. Curr Allergy Asthma Rep 17, 29 (2017). https://doi.org/10.1007/s11882-017-0695-0
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DOI: https://doi.org/10.1007/s11882-017-0695-0