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. 2022 Feb 1:179:388-402.
doi: 10.1016/j.freeradbiomed.2021.10.037. Epub 2021 Nov 14.

Asthma, allergy and vitamin E: Current and future perspectives

Joan M Cook-Mills  1 , Samantha H Averill  2 , Jacquelyn D Lajiness  2
Affiliations

Asthma, allergy and vitamin E: Current and future perspectives

Joan M Cook-Mills et al. Free Radic Biol Med. .

Abstract

Asthma and allergic disease result from interactions of environmental exposures and genetics. Vitamin E is one environmental factor that can modify development of allergy early in life and modify responses to allergen after allergen sensitization. Seemingly varied outcomes from vitamin E are consistent with the differential functions of the isoforms of vitamin E. Mechanistic studies demonstrate that the vitamin E isoforms α-tocopherol and γ-tocopherol have opposite functions in regulation of allergic inflammation and development of allergic disease, with α-tocopherol having anti-inflammatory functions and γ-tocopherol having pro-inflammatory functions in allergy and asthma. Moreover, global differences in prevalence of asthma by country may be a result, at least in part, of differences in consumption of these two isoforms of tocopherols. It is critical in clinical and animal studies that measurements of the isoforms of tocopherols be determined in vehicles for the treatments, and in the plasma and/or tissues before and after intervention. As allergic inflammation is modifiable by tocopherol isoforms, differential regulation by tocopherol isoforms provide a foundation for development of interventions to improve lung function in disease and raise the possibility of early life dietary interventions to limit the development of lung disease.

Keywords: Allergy; Animal models; Asthma; Human; Vitamin E; α-Tocopherol; γ-Tocopherol.

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Figures

Fig. 1.
Fig. 1.
Natural d-tocopherol Isoforms. The most abundant tocopherols in plasma and tissues are α-tocopherol and γ-tocopherol, which differ by one methyl group on the ring.
Fig. 2.
Fig. 2.
During lung development and allergic disease, a balance of levels of α-tocopherol (α–T) and γ-tocopherol (γ–T) are needed to limit disease. Proposed levels are indicated based on levels in countries with low asthma, but additional clinical and mechanistic preclinical studies are needed.
Fig. 3.
Fig. 3.
Maternal α-Tocopherol (α-T) and γ-Tocopherol (γ-T) Supplemented Diets Regulate Development of Allergic Lung Inflammation in Offspring of Allergic Mothers. 90–92.
Fig. 4.
Fig. 4.
Model of α-tocopherol (αT) and γ-tocopherol (γT) regulation of PKC activation during allergic responses. α-T, γT and diacylglycerol compete for binding to the C1A regulatory domain of PKCs. α-T is an antagonist, but γT and diacylglycerol are agonists at the C1A domain during activa-tion of PKCs. PKCα mediates VCAM-1 and ICAM-1 signaling in endothelial cells during leukocyte recruitment in allergic responses. PKCα and PKCδ mediate signals for development of dendritic cells during allergic responses.
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