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10.1016/j.cytogfr.2020.09.002

http://scihub22266oqcxt.onion/10.1016/j.cytogfr.2020.09.002
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32988728!7505161!32988728
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suck abstract from ncbi


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pmid32988728      Cytokine+Growth+Factor+Rev 2021 ; 58 (ä): 102-110
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  • Is Toll-like receptor 4 involved in the severity of COVID-19 pathology in patients with cardiometabolic comorbidities? #MMPMID32988728
  • Brandao SCS; Ramos JOX; Dompieri LT; Godoi ETAM; Figueiredo JL; Sarinho ESC; Chelvanambi S; Aikawa M
  • Cytokine Growth Factor Rev 2021[Apr]; 58 (ä): 102-110 PMID32988728show ga
  • The severe form of COVID-19 is marked by an abnormal and exacerbated immunological host response favoring to a poor outcome in a significant number of patients, especially those with obesity, diabetes, hypertension, and atherosclerosis. The chronic inflammatory process found in these cardiometabolic comorbidities is marked by the overexpression of pro-inflammatory cytokines such as interleukin-6 (IL-6) and tumoral necrosis factor-alpha (TNF-alpha), which are products of the Toll-Like receptors 4 (TLR4) pathway. The SARS-CoV-2 initially infects cells in the upper respiratory tract and, in some patients, spread very quickly, needing respiratory support and systemically, causing collateral damage in tissues. We hypothesize that this happens because the SARS-CoV-2 spike protein interacts strongly with TLR4, causing an intensely exacerbated immune response in the host's lungs, culminating with the cytokine storm, accumulating secretions and hindering blood oxygenation, along with the immune system attacks the body, leading to multiple organ failure.
  • |COVID-19/*complications/epidemiology/pathology[MESH]
  • |Cardiometabolic Risk Factors[MESH]
  • |Cardiovascular Diseases/epidemiology/*etiology[MESH]
  • |Comorbidity[MESH]
  • |Cytokine Release Syndrome/epidemiology/etiology[MESH]
  • |Humans[MESH]
  • |Metabolic Diseases/epidemiology/*etiology[MESH]
  • |Multiple Organ Failure/epidemiology/etiology[MESH]
  • |SARS-CoV-2/*pathogenicity[MESH]
  • |Severity of Illness Index[MESH]


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