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10.3389/fimmu.2020.02014 http://scihub22266oqcxt.onion/10.3389/fimmu.2020.02014 32849666!7432138!32849666     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=32849666&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 500 Internal Server Error in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Immunol 2020 ; 11 (ä): 2014 Nephropedia Template TP {{tp|p=32849666|t=2020. Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key?|pdf=|usr=}}{{32849666}} gab.com Text Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32849666 #FOAvip To date the pathophysiology of COVID-19 remains unclear: this represents a factor determining the current lack of effective treatments. In this paper, we hypothesized a complex host response to SARS-CoV-2, with the Contact System (CS) playing a pivotal role in innate immune response. CS is linked with different proteolytic defense systems operating in human vasculature: the Kallikrein-Kinin (KKS), the Coagulation/Fibrinolysis and the Renin-Angiotensin (RAS) Systems. We investigated the role of the mediators involved. CS consists of Factor XII (FXII) and plasma prekallikrein (complexed to high-molecular-weight kininogen-HK). Autoactivation of FXII by contact with SARS-CoV-2 could lead to activation of intrinsic coagulation, with fibrin formation (microthrombosis), and fibrinolysis, resulting in increased D-dimer levels. Activation of kallikrein by activated FXII leads to production of bradykinin (BK) from HK. BK binds to B2-receptors, mediating vascular permeability, vasodilation and edema. B1-receptors, binding the metabolite [des-Arg(9)]-BK (DABK), are up-regulated during infections and mediate lung inflammatory responses. BK could play a relevant role in COVID-19 as already described for other viral models. Angiotensin-Converting-Enzyme (ACE) 2 displays lung protective effects: it inactivates DABK and converts Angiotensin II (Ang II) into Angiotensin-(1-7) and Angiotensin I into Angiotensin-(1-9). SARS-CoV-2 binds to ACE2 for cell entry, downregulating it: an impaired DABK inactivation could lead to an enhanced activity of B1-receptors, and the accumulation of Ang II, through a negative feedback loop, may result in decreased ACE activity, with consequent increase of BK. Therapies targeting the CS, the KKS and action of BK could be effective for the treatment of COVID-19. Twit Text FOAVip Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=32849666 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32849666 #FOAvip English Wikipedia <ref>{{Cite pmid|32849666}}</ref> Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key? #MMPMID32849666 Meini S; Zanichelli A; Sbrojavacca R; Iuri F; Roberts AT; Suffritti C; Tascini C Front Immunol 2020[]; 11 (ä): 2014 PMID32849666show ga To date the pathophysiology of COVID-19 remains unclear: this represents a factor determining the current lack of effective treatments. In this paper, we hypothesized a complex host response to SARS-CoV-2, with the Contact System (CS) playing a pivotal role in innate immune response. CS is linked with different proteolytic defense systems operating in human vasculature: the Kallikrein-Kinin (KKS), the Coagulation/Fibrinolysis and the Renin-Angiotensin (RAS) Systems. We investigated the role of the mediators involved. CS consists of Factor XII (FXII) and plasma prekallikrein (complexed to high-molecular-weight kininogen-HK). Autoactivation of FXII by contact with SARS-CoV-2 could lead to activation of intrinsic coagulation, with fibrin formation (microthrombosis), and fibrinolysis, resulting in increased D-dimer levels. Activation of kallikrein by activated FXII leads to production of bradykinin (BK) from HK. BK binds to B2-receptors, mediating vascular permeability, vasodilation and edema. B1-receptors, binding the metabolite [des-Arg(9)]-BK (DABK), are up-regulated during infections and mediate lung inflammatory responses. BK could play a relevant role in COVID-19 as already described for other viral models. Angiotensin-Converting-Enzyme (ACE) 2 displays lung protective effects: it inactivates DABK and converts Angiotensin II (Ang II) into Angiotensin-(1-7) and Angiotensin I into Angiotensin-(1-9). SARS-CoV-2 binds to ACE2 for cell entry, downregulating it: an impaired DABK inactivation could lead to an enhanced activity of B1-receptors, and the accumulation of Ang II, through a negative feedback loop, may result in decreased ACE activity, with consequent increase of BK. Therapies targeting the CS, the KKS and action of BK could be effective for the treatment of COVID-19. |Angiotensin-Converting Enzyme 2[MESH] |Betacoronavirus/*metabolism[MESH] |Bradykinin/metabolism[MESH] |COVID-19[MESH] |Capillary Permeability[MESH] |Complement C1 Inhibitor Protein[MESH] |Coronavirus Infections/*immunology/*physiopathology/virology[MESH] |Factor XIIa/metabolism[MESH] |Fibrinolysis/*immunology[MESH] |Host-Pathogen Interactions/immunology[MESH] |Humans[MESH] |Kallikrein-Kinin System/*immunology[MESH] |Kininogen, High-Molecular-Weight/metabolism[MESH] |Pandemics[MESH] |Peptidyl-Dipeptidase A/metabolism[MESH] |Plasma Kallikrein/metabolism[MESH] |Pneumonia, Viral/*immunology/*physiopathology/virology[MESH] |Prekallikrein/metabolism[MESH] |Receptor, Bradykinin B1/metabolism[MESH] |Receptor, Bradykinin B2/metabolism[MESH] |Renin-Angiotensin System/*immunology[MESH] |SARS-CoV-2[MESH]Understanding the Pathophysiology of COVID-19: Could the Contact Syste(epmc).pdf DeepDyve Pubget Overpricing