We are analyzing https://link.springer.com/article/10.1007/s00592-020-01539-z.

Title:
Dipeptidyl peptidase-4 (DPP4) inhibition in COVID-19 | Acta Diabetologica
Description:
Aims SARS–CoV-2 causes severe respiratory syndrome (COVID-19) with high mortality due to a direct cytotoxic viral effect and a severe systemic inflammation. We are herein discussing a possible novel therapeutic tool for COVID-19. Methods Virus binds to the cell surface receptor ACE2; indeed, recent evidences suggested that SARS–CoV-2 may be using as co-receptor, when entering the cells, the same one used by MERS–Co-V, namely the DPP4/CD26 receptor. The aforementioned observation underlined that mechanism of cell entry is supposedly similar among different coronavirus, that the co-expression of ACE2 and DPP4/CD26 could identify those cells targeted by different human coronaviruses and that clinical complications may be similar. Results The DPP4 family/system was implicated in various physiological processes and diseases of the immune system, and DPP4/CD26 is variously expressed on epithelia and endothelia of the systemic vasculature, lung, kidney, small intestine and heart. In particular, DPP4 distribution in the human respiratory tract may facilitate the entrance of the virus into the airway tract itself and could contribute to the development of cytokine storm and immunopathology in causing fatal COVID-19 pneumonia. Conclusions The use of DPP4 inhibitors, such as gliptins, in patients with COVID-19 with, or even without, type 2 diabetes, may offer a simple way to reduce the virus entry and replication into the airways and to hamper the sustained cytokine storm and inflammation within the lung in patients diagnosed with COVID-19 infection.
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Keywords {🔍}

pubmed, google, scholar, cas, dpp, central, covid, peptidase, dipeptidyl, sarscov, human, dppcd, cell, respiratory, coronavirus, article, diabetes, cells, lung, data, patients, syndrome, clinical, inhibitors, inhibition, fiorina, inflammation, virus, receptor, merscov, immune, clin, acta, paolo, severe, similar, storm, activity, treatment, entry, system, cytokine, pneumonia, type, study, milan, diabetic, nature, immunol, italy,

Topics {✒️}

post-translational n-terminal hypersialylation inflammatory monocyte-macrophage responses sars–cov-2 spike glycoprotein cd26-mediated signal transduction cell-dependent immune responses bayesian network meta-analysis dpp4/cd26 transmembrane glycoprotein dipeptidyl peptidase-iv inhibition antagonize sars–cov-2 virulence sars-cov-infected mice severe respiratory syndrome n-glycan binding interfaces emerging human coronavirus-emc t-cell immune response anti-inflammatory effects inhibit dpp4/cd26 activity università di milano impaired tissue remodeling dpp4/cd26 system modulation privacy choices/manage cookies article solerte human coronavirus mers-cov antonio di sabatino insulin-dependent diabetic patients dipeptidyl-peptidase iv dipeptidyl peptidase iv sars–cov-2 binds disabling sars–cov-2 dpp4-mediated induction diffuse vascular leakage glp-1-based therapies porcine respiratory coronavirus dipeptidyl peptidase family dipeptidyl peptidase-4 inhibitors human respiratory tract dipeptidyl peptidase activity cd26/dipeptidyl peptidase-4 sustained cytokine storm important cytokine storm animal rights disclosure san matteo hospital related subjects high mortality due angiotensin-converting enzyme 2 induce alveolar edema glycylproline p-nitroanilide mccray pb jr multiple hemostatic abnormalities left ventricular filling rat asthma model

Questions {❓}

COVID-19: is there a link between the course of infection and pharmacological agents in diabetes?
Cheng XW et al (2018) Dose rectification of an imbalance between DPP4 and GLP-1 ameliorates chronic stress-related vascular aging and atherosclerosis?

Schema {🗺️}

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         description:SARS–CoV-2 causes severe respiratory syndrome (COVID-19) with high mortality due to a direct cytotoxic viral effect and a severe systemic inflammation. We are herein discussing a possible novel therapeutic tool for COVID-19. Virus binds to the cell surface receptor ACE2; indeed, recent evidences suggested that SARS–CoV-2 may be using as co-receptor, when entering the cells, the same one used by MERS–Co-V, namely the DPP4/CD26 receptor. The aforementioned observation underlined that mechanism of cell entry is supposedly similar among different coronavirus, that the co-expression of ACE2 and DPP4/CD26 could identify those cells targeted by different human coronaviruses and that clinical complications may be similar. The DPP4 family/system was implicated in various physiological processes and diseases of the immune system, and DPP4/CD26 is variously expressed on epithelia and endothelia of the systemic vasculature, lung, kidney, small intestine and heart. In particular, DPP4 distribution in the human respiratory tract may facilitate the entrance of the virus into the airway tract itself and could contribute to the development of cytokine storm and immunopathology in causing fatal COVID-19 pneumonia. The use of DPP4 inhibitors, such as gliptins, in patients with COVID-19 with, or even without, type 2 diabetes, may offer a simple way to reduce the virus entry and replication into the airways and to hamper the sustained cytokine storm and inflammation within the lung in patients diagnosed with COVID-19 infection.
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      description:SARS–CoV-2 causes severe respiratory syndrome (COVID-19) with high mortality due to a direct cytotoxic viral effect and a severe systemic inflammation. We are herein discussing a possible novel therapeutic tool for COVID-19. Virus binds to the cell surface receptor ACE2; indeed, recent evidences suggested that SARS–CoV-2 may be using as co-receptor, when entering the cells, the same one used by MERS–Co-V, namely the DPP4/CD26 receptor. The aforementioned observation underlined that mechanism of cell entry is supposedly similar among different coronavirus, that the co-expression of ACE2 and DPP4/CD26 could identify those cells targeted by different human coronaviruses and that clinical complications may be similar. The DPP4 family/system was implicated in various physiological processes and diseases of the immune system, and DPP4/CD26 is variously expressed on epithelia and endothelia of the systemic vasculature, lung, kidney, small intestine and heart. In particular, DPP4 distribution in the human respiratory tract may facilitate the entrance of the virus into the airway tract itself and could contribute to the development of cytokine storm and immunopathology in causing fatal COVID-19 pneumonia. The use of DPP4 inhibitors, such as gliptins, in patients with COVID-19 with, or even without, type 2 diabetes, may offer a simple way to reduce the virus entry and replication into the airways and to hamper the sustained cytokine storm and inflammation within the lung in patients diagnosed with COVID-19 infection.
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