Obesity and COVID-19: immune and metabolic derangement as a possible link to adverse clinical outcomes

Am J Physiol Endocrinol Metab. 2020 Jul 1;319(1):E105-E109. doi: 10.1152/ajpendo.00198.2020. Epub 2020 May 27.

Abstract

Recent reports have shown a strong association between obesity and the severity of COVID-19 infection, even in the absence of other comorbidities. After infecting the host cells, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may cause a hyperinflammatory reaction through the excessive release of cytokines, a condition known as "cytokine storm," while inducing lymphopenia and a disrupted immune response. Obesity is associated with chronic low-grade inflammation and immune dysregulation, but the exact mechanisms through which it exacerbates COVID-19 infection are not fully clarified. The production of increased amounts of cytokines such as TNFα, IL-1, IL-6, and monocyte chemoattractant protein (MCP-1) lead to oxidative stress and defective function of innate and adaptive immunity, whereas the activation of NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome seems to play a crucial role in the pathogenesis of the infection. Endothelial dysfunction and arterial stiffness could favor the recently discovered infection of the endothelium by SARS-CoV-2, whereas alterations in cardiac structure and function and the prothrombotic microenvironment in obesity could provide a link for the increased cardiovascular events in these patients. The successful use of anti-inflammatory agents such as IL-1 and IL-6 blockers in similar hyperinflammatory settings, like that of rheumatoid arthritis, has triggered the discussion of whether such agents could be administrated in selected patients with COVID-19 disease.

Keywords: COVID-19; arterial stiffness; cytokines; immune system; obesity.

Publication types

  • Review

MeSH terms

  • Adaptive Immunity
  • Betacoronavirus
  • COVID-19
  • Coronavirus Infections / immunology
  • Coronavirus Infections / metabolism
  • Coronavirus Infections / physiopathology*
  • Cytokine Release Syndrome / virology
  • Endothelium / physiopathology
  • Heart / physiopathology
  • Heart / virology
  • Humans
  • Immunity, Innate
  • Inflammation
  • NLR Family, Pyrin Domain-Containing 3 Protein / immunology
  • Obesity / virology*
  • Oxidative Stress
  • Pandemics
  • Pneumonia, Viral / immunology
  • Pneumonia, Viral / metabolism
  • Pneumonia, Viral / physiopathology*
  • Risk Factors
  • SARS-CoV-2
  • Thrombosis / physiopathology
  • Vascular Stiffness

Substances

  • NLR Family, Pyrin Domain-Containing 3 Protein
  • NLRP3 protein, human