Immunometabolism at the cornerstone of inflammaging, immunosenescence, and autoimmunity in COVID-19.

Loukman Omarjee,Anne Janin,Olivier Meilhac,Guillaume Mahe,Frédérique Perrot,Guilhem Bousquet

doi:10.18632/aging.202422

Abstract

Inflammaging constitutes the common factor for comorbidities predisposing to severe COVID-19. Inflammaging leads to T-cell senescence, and immunosenescence is linked to autoimmune manifestations in COVID-19. As in SLE, metabolic dysregulation occurs in T-cells. Targeting this T-cell dysfunction opens the field for new therapeutic strategies to prevent severe COVID-19. Immunometabolism-mediated approaches such as rapamycin, metformin and dimethyl fumarate, may optimize COVID-19 treatment of the elderly and patients at risk for severe disease.

Highlights

Chronic low-grade inflammation that develops with aging, termed inflammaging, is a common factor for comorbidities predisposing to severe forms of COVID19 with acute respiratory distress syndrome (ARDS) [1]
A link has been made between immunosenescence in Systemic lupus erythematosus (SLE) patients and immunometabolic alterations such as mitochondrial dysfunction, oxidative stress, glycolysis, glutaminolysis and lipid metabolism contributing to pro-inflammatory T-cell responses [73]
When administered early in the onset of the cytokine storm phase, it is possible that rapamycin prevents progression to severe forms of COVID-19 through the down-regulation of Senescence associated secretory phenotype (SASP), of the mammalian target of the rapamycin (mTOR)-NLR family pyrin domain-containing 3 (NLRP3)-IL-1β axis, of the IL-6 pathway, and of senescent T-cell counts [6]

Summary

Introduction

Chronic low-grade inflammation that develops with aging, termed inflammaging, is a common factor for comorbidities predisposing to severe forms of COVID19 with acute respiratory distress syndrome (ARDS) [1].

Results

Conclusion