Relationship Between Obesity and Immune System a Review Article

el-Fetoh, NagahMohamedAbo; Aodh, AbeerMohmmad; Alanazi, ZainabFarhan; Alenezi, MaramAwied; Alruwaili, MadihahNafea; Alghamdi, RawanSaeed; Alsarawi, HadilMohammad; Almuhawwis, AliGhannam

doi:10.21474/ijar01/2359

Cited by 1 publication

(1 citation statement)

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“…Second, increased levels of lipopolysaccharide and adenosine triphosphate activate the NLRP3 inflammasome, mediating reactive oxygen species (ROS) activation and the release of IL-1β and IL-18 [141]. Third, the activation of M1 macrophages outside of AT is further enhanced by increased secretion of AT inflammatory cytokines TNF-α, IL-6, visfatin, resistin, angiotensin II, and plasminogen activator 1 into the blood [142]. Fourth, the secretion of important adipocytokines in particular leptin impacts the immune response by augmenting the production of TNF-α, IL-6, and IL-12, leading to a predominantly pathogenic proinflammatory T helper type 1 cell (TH1) population [143].…”

Section: Obesity-related Inflammation and Immune Responsesmentioning

confidence: 99%

Obesity and COVID-19: Molecular Mechanisms Linking Both Pandemics

Ritter

Kreis

Louwen

et al. 2020

IJMS

116

122

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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.

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Section: Obesity-related Inflammation and Immune Responsesmentioning

confidence: 99%