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10.3389/fimmu.2021.743890 http://scihub22266oqcxt.onion/10.3389/fimmu.2021.743890 34950134!8688760!34950134     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34950134&cmd=llinks): Failed to open stream: HTTP request failed! 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Imiquimod Boosts Interferon Response, and Decreases ACE2 and Pro-Inflammatory Response of Human Bronchial Epithelium in Asthma |pdf=|usr=}}{{34950134}} gab.com Text Imiquimod Boosts Interferon Response, and Decreases ACE2 and Pro-Inflammatory Response of Human Bronchial Epithelium in Asthma JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34950134 #FOAvip BACKGROUND: Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in ex vivo cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity. OBJECTIVE: To investigate bronchial epithelial effects of imiquimod of potential importance for anti-viral treatment in asthmatic patients. METHODS: Effects of imiquimod alone were examined in HBECs from healthy (N=4) and asthmatic (N=18) donors. Mimicking SARS-CoV-2 infection, HBECs were stimulated with poly(I:C), a dsRNA analogue, or SARS-CoV-2 spike-protein 1 (SP1; receptor binding) with and without imiquimod treatment. Expression of SARS-CoV-2 receptor (ACE2), pro-inflammatory and anti-viral cytokines were analyzed by RT-qPCR, multiplex ELISA, western blot, and Nanostring and proteomic analyses. RESULTS: Imiquimod reduced ACE2 expression at baseline and after poly(I:C) stimulation. Imiquimod also reduced poly(I:C)-induced pro-inflammatory cytokines including IL-1beta, IL-6, IL-8, and IL-33. Furthermore, imiquimod increased IFN-beta expression, an effect potentiated in presence of poly(I:C) or SP1. Multiplex mRNA analysis verified enrichment in type-I IFN signaling concomitant with suppression of cytokine signaling pathways induced by imiquimod in presence of poly(I:C). Exploratory proteomic analyses revealed potentially protective effects of imiquimod on infections. CONCLUSION: Imiquimod triggers viral resistance mechanisms in HBECs by decreasing ACE2 and increasing IFN-beta expression. Additionally, imiquimod improves viral infection tolerance by reducing viral stimulus-induced epithelial cytokines involved in severe COVID-19 infection. Our imiquimod data highlight feasibility of producing pluripotent drugs potentially suited for anti-viral treatment in asthmatic subjects. Twit Text FOAVip Imiquimod Boosts Interferon Response, and Decreases ACE2 and Pro-Inflammatory Response of Human Bronchial Epithelium in Asthma ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34950134 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34950134 #FOAvip English Wikipedia <ref>{{Cite pmid|34950134}}</ref> Imiquimod Boosts Interferon Response, and Decreases ACE2 and Pro-Inflammatory Response of Human Bronchial Epithelium in Asthma #MMPMID34950134 Nieto-Fontarigo JJ; Tillgren S; Cerps S; Sverrild A; Hvidtfeldt M; Ramu S; Menzel M; Sander AF; Porsbjerg C; Uller L Front Immunol 2021[]; 12 (ä): 743890 PMID34950134show ga BACKGROUND: Both anti-viral and anti-inflammatory bronchial effects are warranted to treat viral infections in asthma. We sought to investigate if imiquimod, a TLR7 agonist, exhibits such dual actions in ex vivo cultured human bronchial epithelial cells (HBECs), targets for SARS-CoV-2 infectivity. OBJECTIVE: To investigate bronchial epithelial effects of imiquimod of potential importance for anti-viral treatment in asthmatic patients. METHODS: Effects of imiquimod alone were examined in HBECs from healthy (N=4) and asthmatic (N=18) donors. Mimicking SARS-CoV-2 infection, HBECs were stimulated with poly(I:C), a dsRNA analogue, or SARS-CoV-2 spike-protein 1 (SP1; receptor binding) with and without imiquimod treatment. Expression of SARS-CoV-2 receptor (ACE2), pro-inflammatory and anti-viral cytokines were analyzed by RT-qPCR, multiplex ELISA, western blot, and Nanostring and proteomic analyses. RESULTS: Imiquimod reduced ACE2 expression at baseline and after poly(I:C) stimulation. Imiquimod also reduced poly(I:C)-induced pro-inflammatory cytokines including IL-1beta, IL-6, IL-8, and IL-33. Furthermore, imiquimod increased IFN-beta expression, an effect potentiated in presence of poly(I:C) or SP1. Multiplex mRNA analysis verified enrichment in type-I IFN signaling concomitant with suppression of cytokine signaling pathways induced by imiquimod in presence of poly(I:C). Exploratory proteomic analyses revealed potentially protective effects of imiquimod on infections. CONCLUSION: Imiquimod triggers viral resistance mechanisms in HBECs by decreasing ACE2 and increasing IFN-beta expression. Additionally, imiquimod improves viral infection tolerance by reducing viral stimulus-induced epithelial cytokines involved in severe COVID-19 infection. Our imiquimod data highlight feasibility of producing pluripotent drugs potentially suited for anti-viral treatment in asthmatic subjects. |*Asthma[MESH] |*COVID-19[MESH] |Adjuvants, Immunologic/pharmacology[MESH] |Adult[MESH] |Aged[MESH] |Angiotensin-Converting Enzyme 2/*metabolism[MESH] |Bronchi/drug effects/immunology/virology[MESH] |Cells, Cultured[MESH] |Female[MESH] |Humans[MESH] |Imiquimod/*pharmacology[MESH] |Interferon-beta/*drug effects/immunology[MESH] |Male[MESH] |Middle Aged[MESH] |Respiratory Mucosa/*drug effects/metabolism/virology[MESH]Imiquimod Boosts Interferon Response, and Decreases ACE2 and Pro-Infla(epmc).pdf DeepDyve Pubget Overpricing