Obesity and COVID-19: Molecular Mechanisms Linking Both Pandemics

• Published in: International journal of molecular sciences Vol. 21; no. 16; p. 5793
• Main Authors: Ritter, Andreas, Kreis, Nina-Naomi, Louwen, Frank, Yuan, Juping
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 12.08.2020; MDPI
• Subjects: Adipocytes - metabolism; Adipose tissue; adipose-derived mesenchymal stem/stromal cells; Animals; Cilia; Coronaviridae; Coronavirus Infections - epidemiology; Coronavirus Infections - immunology; Coronaviruses; COVID-19; Cytokine storm; Cytokines; Cytokines - genetics; Cytokines - metabolism; Deregulation; Endothelium; Epithelial cells; Escalators; Fibrosis; Humans; Immune clearance; Immune response; Immune system; Inflammation; Interleukin 6; Lung diseases; Mesenchyme; Molecular modelling; Mortality; Obesity; Obesity - epidemiology; Obesity - immunology; Pandemics; Pathogenesis; Pneumonia, Viral - epidemiology; Pneumonia, Viral - immunology; Public health; Review; Severe acute respiratory syndrome coronavirus 2; Stem cells; Middle East; COVID-19; adipose-derived mesenchymal stem/stromal cells; cytokine storm; immune response; inflammation; obesity
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21165793

The coronavirus disease 2019 COVID-19 pandemic is rapidly spreading worldwide and is becoming a major public health crisis. Increasing evidence demonstrates a strong correlation between obesity and the COVID-19 disease. We have summarized recent studies and addressed the impact of obesity on COVID-19 in terms of hospitalization, severity, mortality, and patient outcome. We discuss the potential molecular mechanisms whereby obesity contributes to the pathogenesis of COVID-19. In addition to obesity-related deregulated immune response, chronic inflammation, endothelium imbalance, metabolic dysfunction, and its associated comorbidities, dysfunctional mesenchymal stem cells/adipose-derived mesenchymal stem cells may also play crucial roles in fueling systemic inflammation contributing to the cytokine storm and promoting pulmonary fibrosis causing lung functional failure, characteristic of severe COVID-19. Moreover, obesity may also compromise motile cilia on airway epithelial cells and impair functioning of the mucociliary escalators, reducing the clearance of severe acute respiratory syndrome coronavirus (SARS-CoV-2). Obese diseased adipose tissues overexpress the receptors and proteases for the SARS-CoV-2 entry, implicating its possible roles as virus reservoir and accelerator reinforcing violent systemic inflammation and immune response. Finally, anti-inflammatory cytokines like anti-interleukin 6 and administration of mesenchymal stromal/stem cells may serve as potential immune modulatory therapies for supportively combating COVID-19. Obesity is conversely related to the development of COVID-19 through numerous molecular mechanisms and individuals with obesity belong to the COVID-19-susceptible population requiring more protective measures.