PropertyValue
?:abstract
  • Although some evidence showed the activation of complement systems in COVID-19 patients, proinflammatory status and lectin pathway remain unclear Thus, the present study aimed to demonstrate the role of MBL and ficolin-3 in the complement system activation and compared to pandemic Influenza A virus H1N1 subtype infection (H1N1pdm09) and control patients A total of 27 lungs formalin-fixed paraffin-embedded (FFPE) samples (10 from H1N1 group, 6 from the COVID-19 group, and 11 from the control group) were analyzed by immunohistochemistry using anti-IL-6, TNF-alfa, CD163, MBL e FCN3 antibodies Genotyping of target polymorphisms in the MBL2 gene was performed by real-time PCR Proinflammatory cytokines such as IL-6 and TNF-alpha presented higher tissue expression in the COVID-19 group compared to H1N1 and control groups The same results were observed for ICAM-1 tissue expression Increased expression of the FCN3 was observed in the COVID-19 group and H1N1 group compared to the control group The MBL tissue expression was higher in the COVID-19 group compared to H1N1 and control groups The genotypes AA for rs180040 (G/A), GG for rs1800451 (G/A) and CC for rs5030737 (T/C) showed a higher prevalence in the COVID-19 group The intense activation of the lectin pathway, with particular emphasis on the MBL pathway, together with endothelial dysfunction and a massive proinflammatory cytokines production, possibly lead to a worse outcome in patients infected with SARS-Cov-2 Moreover, 3 SNPs of our study presented genotypes that might be correlated with high MBL tissue expression in the COVID-19 pulmonary samples
is ?:annotates of
?:creator
?:journal
  • Transl_Res
?:license
  • unk
?:publication_isRelatedTo_Disease
is ?:relation_isRelatedTo_publication of
?:source
  • WHO
?:title
  • The role of the lectin pathway of the complement system in SARS-CoV-2 lung injury
?:type
?:who_covidence_id
  • #939331
?:year
  • 2020

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