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10.1016/j.immuni.2021.04.001 http://scihub22266oqcxt.onion/10.1016/j.immuni.2021.04.001 33951416!8192557!33951416     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Immunity 2021 ; 54 (6): 1200-1218.e9 Nephropedia Template TP {{tp|p=33951416|t=2021. Uncoupling of macrophage inflammation from self-renewal modulates host recovery from respiratory viral infection |pdf=|usr=}}{{33951416}} gab.com Text Uncoupling of macrophage inflammation from self-renewal modulates host recovery from respiratory viral infection JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=33951416 #FOAvip Tissue macrophages self-renew during homeostasis and produce inflammatory mediators upon microbial infection. We examined the relationship between proliferative and inflammatory properties of tissue macrophages by defining the impact of the Wnt/beta-catenin pathway, a central regulator of self-renewal, in alveolar macrophages (AMs). Activation of beta-catenin by Wnt ligand inhibited AM proliferation and stemness, but promoted inflammatory activity. In a murine influenza viral pneumonia model, beta-catenin-mediated AM inflammatory activity promoted acute host morbidity; in contrast, AM proliferation enabled repopulation of reparative AMs and tissue recovery following viral clearance. Mechanistically, Wnt treatment promoted beta-catenin-HIF-1alpha interaction and glycolysis-dependent inflammation while suppressing mitochondrial metabolism and thereby, AM proliferation. Differential HIF-1alpha activities distinguished proliferative and inflammatory AMs in vivo. This beta-catenin-HIF-1alpha axis was conserved in human AMs and enhanced HIF-1alpha expression associated with macrophage inflammation in COVID-19 patients. Thus, inflammatory and reparative activities of lung macrophages are regulated by beta-catenin-HIF-1alpha signaling, with implications for the treatment of severe respiratory diseases. Twit Text FOAVip Uncoupling of macrophage inflammation from self-renewal modulates host recovery from respiratory viral infection ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=33951416 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33951416 #FOAvip English Wikipedia <ref>{{Cite pmid|33951416}}</ref> Uncoupling of macrophage inflammation from self-renewal modulates host recovery from respiratory viral infection #MMPMID33951416 Zhu B; Wu Y; Huang S; Zhang R; Son YM; Li C; Cheon IS; Gao X; Wang M; Chen Y; Zhou X; Nguyen Q; Phan AT; Behl S; Taketo MM; Mack M; Shapiro VS; Zeng H; Ebihara H; Mullon JJ; Edell ES; Reisenauer JS; Demirel N; Kern RM; Chakraborty R; Cui W; Kaplan MH; Zhou X; Goldrath AW; Sun J Immunity 2021[Jun]; 54 (6): 1200-1218.e9 PMID33951416show ga Tissue macrophages self-renew during homeostasis and produce inflammatory mediators upon microbial infection. We examined the relationship between proliferative and inflammatory properties of tissue macrophages by defining the impact of the Wnt/beta-catenin pathway, a central regulator of self-renewal, in alveolar macrophages (AMs). Activation of beta-catenin by Wnt ligand inhibited AM proliferation and stemness, but promoted inflammatory activity. In a murine influenza viral pneumonia model, beta-catenin-mediated AM inflammatory activity promoted acute host morbidity; in contrast, AM proliferation enabled repopulation of reparative AMs and tissue recovery following viral clearance. Mechanistically, Wnt treatment promoted beta-catenin-HIF-1alpha interaction and glycolysis-dependent inflammation while suppressing mitochondrial metabolism and thereby, AM proliferation. Differential HIF-1alpha activities distinguished proliferative and inflammatory AMs in vivo. This beta-catenin-HIF-1alpha axis was conserved in human AMs and enhanced HIF-1alpha expression associated with macrophage inflammation in COVID-19 patients. Thus, inflammatory and reparative activities of lung macrophages are regulated by beta-catenin-HIF-1alpha signaling, with implications for the treatment of severe respiratory diseases. |Biomarkers[MESH] |COVID-19/*immunology/metabolism/*virology[MESH] |Cell Self Renewal/*immunology[MESH] |Cytokines/metabolism[MESH] |Disease Susceptibility/immunology[MESH] |Host-Pathogen Interactions/*immunology[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/metabolism[MESH] |Inflammation Mediators/metabolism[MESH] |Macrophages, Alveolar/immunology/metabolism[MESH] |Macrophages/cytology/*immunology/metabolism[MESH] |SARS-CoV-2/*immunology[MESH]Uncoupling of macrophage inflammation from self-renewal modulates host(epmc).pdf DeepDyve Pubget Overpricing