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10.3389/fimmu.2021.791753 http://scihub22266oqcxt.onion/10.3389/fimmu.2021.791753 34950152!8688532!34950152     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34950152&cmd=llinks): Failed to open stream: HTTP request failed! 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SARS-CoV-2 N Protein Induces Acute Lung Injury in Mice via NF-kB Activation |pdf=|usr=}}{{34950152}} gab.com Text SARS-CoV-2 N Protein Induces Acute Lung Injury in Mice via NF-kB Activation JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34950152 #FOAvip BACKGROUND: Infection of SARS-CoV-2 may cause acute respiratory syndrome. It has been reported that SARS-CoV-2 nucleocapsid protein (N-protein) presents early in body fluids during infection. The direct involvement of N-protein in lung injury is poorly understood. METHODS: Recombinant N-protein was pretreated with polymyxin B, a lipopolysaccharide (LPS)-neutralizing agent. C57BL/6, C3H/HeJ (resistant to LPS), and C3H/HeN (control for C3H/HeJ) mice were exposed to N-protein via intratracheal administration to examine acute lung injury. In vitro, bone marrow-derived macrophages (BMDMs) were cultured with N-protein to study phosphorylation of nuclear factor kappa B (NF-kB) p65, macrophage polarization, and expression of proinflammatory cytokines. RESULTS: N-protein produced acute lung injury in C57BL/6 mice, with elevated protein permeability, total cell count, neutrophil infiltration, and proinflammatory cytokines in the bronchioalveolar lavage. N-protein also induced lung injury in both C3H/HeJ and C3H/HeN mice, indicating that the effect could not be attributed to the LPS contamination. N-protein triggered phosphorylation of NF-kB p65 in vitro, which was abolished by both N-protein denaturation and treatment with an antibody for N-protein, demonstrating that the effect is N-protein specific. In addition, N-protein promoted M1 macrophage polarization and the expression of proinflammatory cytokines, which was also blocked by N-protein denaturation and antibody for N-protein. Furthermore, N-protein induced NF-kB p65 phosphorylation in the lung, while pyrrolidine dithiocarbamate, an NF-kB inhibitor, alleviated the effect of N-protein on acute lung injury. CONCLUSIONS: SARS-CoV-2 N-protein itself is toxic and induces acute lung injury in mice. Both N-protein and NF-kB pathway may be therapeutic targets for treating multi-organ injuries in Coronavirus disease 2019 (COVID-19). Twit Text FOAVip SARS-CoV-2 N Protein Induces Acute Lung Injury in Mice via NF-kB Activation ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34950152 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34950152 #FOAvip English Wikipedia <ref>{{Cite pmid|34950152}}</ref> SARS-CoV-2 N Protein Induces Acute Lung Injury in Mice via NF-kB Activation #MMPMID34950152 Xia J; Tang W; Wang J; Lai D; Xu Q; Huang R; Hu Y; Gong X; Fan J; Shu Q; Xu J Front Immunol 2021[]; 12 (ä): 791753 PMID34950152show ga BACKGROUND: Infection of SARS-CoV-2 may cause acute respiratory syndrome. It has been reported that SARS-CoV-2 nucleocapsid protein (N-protein) presents early in body fluids during infection. The direct involvement of N-protein in lung injury is poorly understood. METHODS: Recombinant N-protein was pretreated with polymyxin B, a lipopolysaccharide (LPS)-neutralizing agent. C57BL/6, C3H/HeJ (resistant to LPS), and C3H/HeN (control for C3H/HeJ) mice were exposed to N-protein via intratracheal administration to examine acute lung injury. In vitro, bone marrow-derived macrophages (BMDMs) were cultured with N-protein to study phosphorylation of nuclear factor kappa B (NF-kB) p65, macrophage polarization, and expression of proinflammatory cytokines. RESULTS: N-protein produced acute lung injury in C57BL/6 mice, with elevated protein permeability, total cell count, neutrophil infiltration, and proinflammatory cytokines in the bronchioalveolar lavage. N-protein also induced lung injury in both C3H/HeJ and C3H/HeN mice, indicating that the effect could not be attributed to the LPS contamination. N-protein triggered phosphorylation of NF-kB p65 in vitro, which was abolished by both N-protein denaturation and treatment with an antibody for N-protein, demonstrating that the effect is N-protein specific. In addition, N-protein promoted M1 macrophage polarization and the expression of proinflammatory cytokines, which was also blocked by N-protein denaturation and antibody for N-protein. Furthermore, N-protein induced NF-kB p65 phosphorylation in the lung, while pyrrolidine dithiocarbamate, an NF-kB inhibitor, alleviated the effect of N-protein on acute lung injury. CONCLUSIONS: SARS-CoV-2 N-protein itself is toxic and induces acute lung injury in mice. Both N-protein and NF-kB pathway may be therapeutic targets for treating multi-organ injuries in Coronavirus disease 2019 (COVID-19). |*COVID-19[MESH] |Acute Lung Injury/metabolism/*virology[MESH] |Animals[MESH] |Coronavirus Nucleocapsid Proteins/*toxicity[MESH] |Mice[MESH] |Mice, Inbred C3H[MESH] |Mice, Inbred C57BL[MESH] |NF-kappa B/*metabolism[MESH] |Phosphoproteins/toxicity[MESH]SARS-CoV-2 N Protein Induces Acute Lung Injury in Mice via NF-kB Activ(epmc).pdf DeepDyve Pubget Overpricing