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10.3389/fcimb.2021.655666 http://scihub22266oqcxt.onion/10.3389/fcimb.2021.655666 33981629!8107375!33981629     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 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Cell+Infect+Microbiol 2021 ; 11 (ä): 655666 Nephropedia Template TP {{tp|p=33981629|t=2021. Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells |pdf=|usr=}}{{33981629}} gab.com Text Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells JO: Front Cell Infect Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=33981629 #FOAvip BACKGROUND: From the first detection in 2019, SARS-CoV-2 infections have spread rapidly worldwide and have been proven to cause an urgent and important health problem. SARS-CoV-2 cell entry depends on two proteins present on the surface of host cells, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). The nasal cavity is thought to be one of the initial sites of infection and a possible reservoir for dissemination within and between individuals. However, it is not known how the expression of these genes is regulated in the nasal mucosa. OBJECTIVE: In this study, we examined whether the expression of ACE2 and TMPRSS2 is affected by innate immune signals in the nasal mucosa. We also investigated how fluticasone propionate (FP), a corticosteroid used as an intranasal steroid spray, affects the gene expression. METHODS: Primary human nasal epithelial cells (HNECs) were collected from the nasal mucosa and incubated with Toll-like receptor (TLR) agonists and/or fluticasone propionate (FP), followed by quantitative PCR, immunofluorescence, and immunoblot analyses. RESULTS: Among the TLR agonists, the TLR3 agonist Poly(I:C) significantly increased ACE2 and TMPRSS2 mRNA expression in HNECs (ACE2 36.212+/-11.600-fold change, p<0.0001; TMPRSS2 5.598+/-2.434-fold change, p=0.031). The ACE2 protein level was also increased with Poly(I:C) stimulation (2.884+/-0.505-fold change, p=0.003). The Poly(I:C)-induced ACE2 expression was suppressed by co-incubation with FP (0.405+/-0.312-fold change, p=0.044). CONCLUSION: The activation of innate immune signals via TLR3 promotes the expression of genes related to SARS-CoV2 cell entry in the nasal mucosa, although this expression is suppressed in the presence of FP. Further studies are required to evaluate whether FP suppresses SARS-CoV-2 viral cell entry. Twit Text FOAVip Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells ????Front Cell Infect Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=33981629 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33981629 #FOAvip English Wikipedia <ref>{{Cite pmid|33981629}}</ref> Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells #MMPMID33981629 Nakazono A; Nakamaru Y; Ramezanpour M; Kondo T; Watanabe M; Hatakeyama S; Kimura S; Honma A; Wormald PJ; Vreugde S; Suzuki M; Homma A Front Cell Infect Microbiol 2021[]; 11 (ä): 655666 PMID33981629show ga BACKGROUND: From the first detection in 2019, SARS-CoV-2 infections have spread rapidly worldwide and have been proven to cause an urgent and important health problem. SARS-CoV-2 cell entry depends on two proteins present on the surface of host cells, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). The nasal cavity is thought to be one of the initial sites of infection and a possible reservoir for dissemination within and between individuals. However, it is not known how the expression of these genes is regulated in the nasal mucosa. OBJECTIVE: In this study, we examined whether the expression of ACE2 and TMPRSS2 is affected by innate immune signals in the nasal mucosa. We also investigated how fluticasone propionate (FP), a corticosteroid used as an intranasal steroid spray, affects the gene expression. METHODS: Primary human nasal epithelial cells (HNECs) were collected from the nasal mucosa and incubated with Toll-like receptor (TLR) agonists and/or fluticasone propionate (FP), followed by quantitative PCR, immunofluorescence, and immunoblot analyses. RESULTS: Among the TLR agonists, the TLR3 agonist Poly(I:C) significantly increased ACE2 and TMPRSS2 mRNA expression in HNECs (ACE2 36.212+/-11.600-fold change, p<0.0001; TMPRSS2 5.598+/-2.434-fold change, p=0.031). The ACE2 protein level was also increased with Poly(I:C) stimulation (2.884+/-0.505-fold change, p=0.003). The Poly(I:C)-induced ACE2 expression was suppressed by co-incubation with FP (0.405+/-0.312-fold change, p=0.044). CONCLUSION: The activation of innate immune signals via TLR3 promotes the expression of genes related to SARS-CoV2 cell entry in the nasal mucosa, although this expression is suppressed in the presence of FP. Further studies are required to evaluate whether FP suppresses SARS-CoV-2 viral cell entry. |*COVID-19[MESH] |*Peptidyl-Dipeptidase A/genetics[MESH] |Angiotensin-Converting Enzyme 2[MESH] |Epithelial Cells[MESH] |Fluticasone[MESH] |Humans[MESH] |RNA, Viral[MESH]Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Hu(epmc).pdf DeepDyve Pubget Overpricing