Cellular metabolism and hypoxia interfacing with allergic diseases

Author:

Kellett Shauna K1,Masterson Joanne C123

Affiliation:

1. Allergy, Inflammation & Remodelling Research Laboratory, Department of Biology, Maynooth University , Maynooth, W23 C2N1, County Kildare , Ireland

2. Gastrointestinal Eosinophilic Diseases Program, Department of Paediatrics, Digestive Health Institute, Children's Hospital Colorado, University of Colorado School of Medicine , Aurora, CO , United States

3. Kathleen Lonsdale Institute for Human Health Research, Maynooth University , Maynooth, W23 C2N1, County Kildare , Ireland

Abstract

Abstract Allergic diseases display significant heterogeneity in their pathogenesis. Understanding the influencing factors, pathogenesis, and advancing new treatments for allergic diseases is becoming more and more vital as currently, prevalence continues to rise, and mechanisms of allergic diseases are not fully understood. The upregulation of the hypoxia response is linked to an elevated infiltration of activated inflammatory cells, accompanied by elevated metabolic requirements. An enhanced hypoxia response may potentially contribute to inflammation, remodeling, and the onset of allergic diseases. It has become increasingly clear that the process underlying immune and stromal cell activation during allergic sensitization requires well-tuned and dynamic changes in cellular metabolism. The purpose of this review is to examine current perspectives regarding metabolic dysfunction in allergic diseases. In the past decade, new technological platforms such as “omic” techniques have been applied, allowing for the identification of different biomarkers in multiple models ranging from altered lipid species content, increased nutrient transporters, and altered serum amino acids in various allergic diseases. Better understanding, recognition, and integration of these alterations would increase our knowledge of pathogenesis and potentially actuate a novel repertoire of targeted treatment approaches that regulate immune metabolic pathways.

Funder

Science Foundation Ireland

Health Research Board

Publisher

Oxford University Press (OUP)

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