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10.1016/j.trsl.2020.11.008

http://scihub22266oqcxt.onion/10.1016/j.trsl.2020.11.008
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33221483!7677075!33221483
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suck abstract from ncbi


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pmid33221483      Transl+Res 2021 ; 231 (ä): 55-63
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  • The role of the lectin pathway of the complement system in SARS-CoV-2 lung injury #MMPMID33221483
  • Malaquias MAS; Gadotti AC; Motta-Junior JDS; Martins APC; Azevedo MLV; Benevides APK; Cezar-Neto P; Panini do Carmo LA; Zeni RC; Raboni SM; Fonseca AS; Machado-Souza C; Moreno-Amaral AN; de Noronha L
  • Transl Res 2021[May]; 231 (ä): 55-63 PMID33221483show ga
  • 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 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.
  • |*SARS-CoV-2[MESH]
  • |Adult[MESH]
  • |Aged[MESH]
  • |Aged, 80 and over[MESH]
  • |Autopsy[MESH]
  • |COVID-19/*pathology[MESH]
  • |Case-Control Studies[MESH]
  • |Complement Activation/physiology[MESH]
  • |Cytokines/genetics/metabolism[MESH]
  • |Female[MESH]
  • |Genotype[MESH]
  • |Humans[MESH]
  • |Immunohistochemistry[MESH]
  • |Influenza A Virus, H1N1 Subtype[MESH]
  • |Influenza, Human/metabolism/pathology[MESH]
  • |Lectins/*metabolism[MESH]
  • |Lung Injury/*metabolism/*pathology/virology[MESH]
  • |Lung/pathology/virology[MESH]
  • |Male[MESH]
  • |Middle Aged[MESH]
  • |Polymorphism, Single Nucleotide[MESH]


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