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Article ; Online: Dipeptidyl peptidase-4 (DPP4) inhibition in COVID-19.

Solerte, Sebastiano Bruno / Di Sabatino, Antonio / Galli, Massimo / Fiorina, Paolo

2020 Volume 57, Issue 7, Page(s) 779–783

Abstract: ... 19 pneumonia.: Conclusions: The use of DPP4 inhibitors, such as gliptins, in patients with COVID ... Aims: SARS-CoV-2 causes severe respiratory syndrome (COVID-19) with high mortality due to a direct ... therapeutic tool for COVID-19.: Methods: Virus binds to the cell surface receptor ACE2; indeed, recent ...

Abstract	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.
MeSH term(s)	Betacoronavirus ; COVID-19 ; Coronavirus Infections/drug therapy ; Coronavirus Infections/enzymology ; Dipeptidyl Peptidase 4/drug effects ; Dipeptidyl Peptidase 4/metabolism ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Humans ; Lung/metabolism ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/enzymology ; SARS-CoV-2
Chemical Substances	Dipeptidyl-Peptidase IV Inhibitors ; Dipeptidyl Peptidase 4 (EC 3.4.14.5)
Keywords	covid19
Language	English
Publishing date	2020-06-06
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	1097676-0
ISSN	1432-5233 ; 0940-5429
ISSN (online)	1432-5233
ISSN	0940-5429
DOI	10.1007/s00592-020-01539-z
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Article ; Online: Dipeptidyl peptidase-4 (DPP4) inhibition in COVID-19

Solerte, Sebastiano Bruno / Di Sabatino, Antonio / Galli, Massimo / Fiorina, Paolo

Acta Diabetologica

2020 Volume 57, Issue 7, Page(s) 779–783

Keywords	Internal Medicine ; Endocrinology, Diabetes and Metabolism ; Endocrinology ; General Medicine ; covid19
Language	English
Publisher	Springer Science and Business Media LLC
Publishing country	us
Document type	Article ; Online
ZDB-ID	1097676-0
ISSN	1432-5233 ; 0940-5429
ISSN (online)	1432-5233
ISSN	0940-5429
DOI	10.1007/s00592-020-01539-z
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Article ; Online: Dipeptidyl peptidase-4 (DPP4) inhibition in COVID-19

S.B. Solerte / A. Di Sabatino / M. Galli / P. Fiorina

2020

Abstract: ... Conclusions: The use of DPP4 inhibitors, such as gliptins, in patients with COVID-19 with, or even ... Aims: SARS–CoV-2 causes severe respiratory syndrome (COVID-19) with high mortality due to a direct ... therapeutic tool for COVID-19. Methods: Virus binds to the cell surface receptor ACE2; indeed, recent ...

Abstract	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.
Keywords	Cytokine storm ; Diabetes ; DPP4 inhibitors ; Pneumonia ; SARS–CoV-2 ; Settore MED/17 - Malattie Infettive ; Settore MED/13 - Endocrinologia ; covid19
Language	English
Publisher	Springer
Publishing country	it
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Dipeptidyl peptidase-4 (DPP4) inhibition in COVID-19

Solerte, S. B. / Di Sabatino, A. / Galli, M. / Fiorina, P.

2020

Abstract	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.
Keywords	Cytokine storm ; Diabetes ; DPP4 inhibitors ; Pneumonia ; SARS–CoV-2 ; covid19
Subject code	616
Language	English
Publishing country	it
Document type	Article ; Online
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Article: Dipeptidyl peptidase-4 (DPP4) inhibition in COVID-19

Solerte, Sebastiano Bruno / Di Sabatino, Antonio / Galli, Massimo / Fiorina, Paolo

Acta Diabetol

Abstract: ... CONCLUSIONS: The use of DPP4 inhibitors, such as gliptins, in patients with COVID-19 with, or even ... AIMS: SARS-CoV-2 causes severe respiratory syndrome (COVID-19) with high mortality due to a direct ... therapeutic tool for COVID-19. METHODS: Virus binds to the cell surface receptor ACE2; indeed, recent ...

Abstract	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.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #549301
Database	COVID19

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Article ; Online: Diabetic individuals with COVID-19 exhibit reduced efficacy of gliptins in inhibiting dipeptidyl peptidase 4 (DPP4). A suggested explanation for increased COVID-19 susceptibility in patients with type 2 diabetes mellitus (T2DM).

Mora-Rodríguez, José María / Sánchez, Belén G / Bort, Alicia / Díaz-Yuste, Alba / Ballester-González, Rubén / Arrieta, Francisco / Sebastián-Martín, Alba / Díaz-Laviada, Inés

Life sciences

2023 Volume 336, Page(s) 122292

Abstract: Aims: Dipeptidyl peptidase 4 (DPP4) has been proposed as a coreceptor for SARS-CoV-2 cellular ... this study aims to unravel the impact of DPP4 in the intersection of T2DM/COVID-19.: Materials and methods ... 19, COVID-19 + T2DM, and COVID-19 + T2DM + gliptins), measuring DPP4 protein concentration and ...

Abstract	Aims: Dipeptidyl peptidase 4 (DPP4) has been proposed as a coreceptor for SARS-CoV-2 cellular entry. Considering that type 2 diabetes mellitus (T2DM) has been identified as the most important risk factor for SARS-CoV-2, and that gliptins (DPP4 inhibitors) are a prescribed diabetic treatment, this study aims to unravel the impact of DPP4 in the intersection of T2DM/COVID-19. Materials and methods: We analyzed 189 serum human samples, divided into six clinical groups (controls, T2DM, T2DM + gliptins, COVID-19, COVID-19 + T2DM, and COVID-19 + T2DM + gliptins), measuring DPP4 protein concentration and activity by Western blot, ELISA, and commercial activity kits. The obtained results were verified in Huh-7 cellular models. Key findings: Both DPP4 concentration and activity were decreased in COVID-19 patients, and as in T2DM patients, compared to controls. Despite these lower levels, the ratio of DPP4 activity/concentration in COVID-19 sera was the highest (0.782 ± 0.289 μU/ng vs. 0.547 ± 0.050 μU/ng in controls, p < 0.0001), suggesting a compensating mechanism in these patients. Supernatants of Huh-7 cells incubated with COVID-19 serum showed a consistent and significantly lower DPP4 concentration and activity. Furthermore, COVID-19 + T2DM + gliptins patients showed a higher serum DPP4 concentration and activity than T2DM + gliptin subjects (p < 0.05), indicating that sera from COVID-19 convalescents interfere with gliptins. Significance: Either SARS-CoV-2 or some metabolites present in the sera of COVID-19-convalescent patients interact with soluble DPP4 or even gliptins themselves since the inhibitory effect of gliptins on DPP4 activity is being prevented. The interactions between DPP4, gliptins, and SARS-CoV-2 should be further elucidated to reveal the mechanism of action for these interesting observations.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; COVID-19 ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Dipeptidyl-Peptidase IV Inhibitors/therapeutic use ; Dipeptidyl Peptidase 4/metabolism ; SARS-CoV-2/metabolism
Chemical Substances	Dipeptidyl-Peptidase IV Inhibitors ; Dipeptidyl Peptidase 4 (EC 3.4.14.5)
Language	English
Publishing date	2023-11-27
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2023.122292
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Uc I Zs.368: Show issues

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Article ; Online: The many facets of CD26/dipeptidyl peptidase 4 and its inhibitors in disorders of the CNS - a critical overview.

Bernstein, Hans-Gert / Keilhoff, Gerburg / Dobrowolny, Henrik / Steiner, Johann

Reviews in the neurosciences

2022 Volume 34, Issue 1, Page(s) 1–24

Abstract: Dipeptidyl peptidase 4 is a serine protease that cleaves X-proline or X-alanine in the penultimate ... For a number of diseases (Covid-19 infection, type 2 diabetes, Alzheimer disease, vascular dementia ... homeostasis and regulation of the immune system. It is expressed in many organs including the brain. DPP4 ...

Abstract	Dipeptidyl peptidase 4 is a serine protease that cleaves X-proline or X-alanine in the penultimate position. Natural substrates of the enzyme are glucagon-like peptide-1, glucagon inhibiting peptide, glucagon, neuropeptide Y, secretin, substance P, pituitary adenylate cyclase-activating polypeptide, endorphins, endomorphins, brain natriuretic peptide, beta-melanocyte stimulating hormone and amyloid peptides as well as some cytokines and chemokines. The enzyme is involved in the maintenance of blood glucose homeostasis and regulation of the immune system. It is expressed in many organs including the brain. DPP4 activity may be effectively depressed by DPP4 inhibitors. Apart from enzyme activity, DPP4 acts as a cell surface (co)receptor, associates with adeosine deaminase, interacts with extracellular matrix, and controls cell migration and differentiation. This review aims at revealing the impact of DPP4 and DPP4 inhibitors for several brain diseases (virus infections affecting the brain, tumours of the CNS, neurological and psychiatric disorders). Special emphasis is given to a possible involvement of DPP4 expressed in the brain.While prominent contributions of extracerebral DPP4 are evident for a majority of diseases discussed herein; a possible role of "brain" DPP4 is restricted to brain cancers and Alzheimer disease. For a number of diseases (Covid-19 infection, type 2 diabetes, Alzheimer disease, vascular dementia, Parkinson disease, Huntington disease, multiple sclerosis, stroke, and epilepsy), use of DPP4 inhibitors has been shown to have a disease-mitigating effect. However, these beneficial effects should mostly be attributed to the depression of "peripheral" DPP4, since currently used DPP4 inhibitors are not able to pass through the intact blood-brain barrier.
MeSH term(s)	Humans ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Dipeptidyl-Peptidase IV Inhibitors/therapeutic use ; Dipeptidyl Peptidase 4/metabolism ; Diabetes Mellitus, Type 2 ; Glucagon ; COVID-19 ; Alzheimer Disease
Chemical Substances	Dipeptidyl-Peptidase IV Inhibitors ; Dipeptidyl Peptidase 4 (EC 3.4.14.5) ; Glucagon (9007-92-5)
Language	English
Publishing date	2022-07-01
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	639035-3
ISSN	2191-0200 ; 0334-1763
ISSN (online)	2191-0200
ISSN	0334-1763
DOI	10.1515/revneuro-2022-0026
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Article: The many facets of CD26/dipeptidyl peptidase 4 and its inhibitors in disorders of the CNS - A critical overview

Bernstein, Hans-Gert / Keilhoff, Gerburg / Dobrowolny, Henrik / Steiner, Johann

Reviews in the Neurosciences

2023 Volume 34, Issue 1, Page(s) 1–24

Title translation	Die vielen Facetten von CD26/Dipeptidylpeptidase 4 und ihren Inhibitoren bei Erkrankungen des ZNS - Ein kritischer Überblick
Abstract	Dipeptidyl peptidase 4 is a serine protease that cleaves X-proline or X-alanine in the penultimate position. Natural substrates of the enzyme are glucagon-like peptide-1, glucagon inhibiting peptide, glucagon, neuropeptide Y, secretin, substance P, pituitary adenylate cyclase-activating polypeptide, endorphins, endomorphins, brain natriuretic peptide, beta-melanocyte stimulating hormone and amyloid peptides as well as some cytokines and chemokines. The enzyme is involved in the maintenance of blood glucose homeostasis and regulation of the immune system. It is expressed in many organs including the brain. DPP4 activity may be effectively depressed by DPP4 inhibitors. Apart from enzyme activity, DPP4 acts as a cell surface (co)receptor, associates with adeosine deaminase, interacts with extracellular matrix, and controls cell migration and differentiation. This review aims at revealing the impact of DPP4 and DPP4 inhibitors for several brain diseases (virus infections affecting the brain, tumours of the CNS, neurological and psychiatric disorders). Special emphasis is given to a possible involvement of DPP4 expressed in the brain.While prominent contributions of extracerebral DPP4 are evident for a majority of diseases discussed herein; a possible role of "brain" DPP4 is restricted to brain cancers and Alzheimer disease. For a number of diseases (Covid-19 infection, type 2 diabetes, Alzheimer disease, vascular dementia, Parkinson disease, Huntington disease, multiple sclerosis, stroke, and epilepsy), use of DPP4 inhibitors has been shown to have a disease-mitigating effect. However, these beneficial effects should mostly be attributed to the depression of "peripheral" DPP4, since currently used DPP4 inhibitors are not able to pass through the intact blood-brain barrier.
Keywords	Brain Neoplasms ; COVID-19 ; Central Nervous System ; Central Nervous System Disorders ; Enzyme ; Enzymes ; Erkrankungen des zentralen Nervensystems ; Hirntumore ; Mental Disorders ; Middle East Respiratory Syndrome ; Proteine ; Proteins ; Psychische Störungen ; Zentrales Nervensystem
Language	English
Document type	Article
ZDB-ID	639035-3
ISSN	2191-0200 ; 0334-1763
ISSN (online)	2191-0200
ISSN	0334-1763
DOI	10.1515/revneuro-2022-0026
Database	PSYNDEX

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Article ; Online: Dipeptidylpeptidase (DPP)-4 inhibitor therapy increases circulating levels of anti-inflammatory soluble frizzle receptor protein (sFRP)-5 which is decreased in severe COVID-19 disease.

Brandes, Juliane / Zobel, Isabelle / Rohmann, Nathalie / Schlicht, Kristina / Geisler, Corinna / Hartmann, Katharina / Türk, Kathrin / von Schönfels, Witigo / Beckmann, Jan / Tran, Florian / Laudes, Matthias

Scientific reports

2022 Volume 12, Issue 1, Page(s) 14935

Abstract: ... in relation to DPP4 inhibition. sFRP5 is a specific antagonist to Wnt5a, a glycopeptide secreted ... Obesity and type 2 diabetes (T2D) show an increased risk for a severe COVID-19 disease. Treatment ... to identify potential mechanisms for the observed DPP4i effect in COVID-19. Comparing T2D subjects with and ...

Abstract	Obesity and type 2 diabetes (T2D) show an increased risk for a severe COVID-19 disease. Treatment with DPP4 inhibitor (DPP4i) results in reduced mortality and better clinical outcome. Here, we aimed to identify potential mechanisms for the observed DPP4i effect in COVID-19. Comparing T2D subjects with and without DPP4i treatment, we identified a significant increase of the anti-inflammatory adipokine sFRP5 in relation to DPP4 inhibition. sFRP5 is a specific antagonist to Wnt5a, a glycopeptide secreted by adipose tissue macrophages acting pro-inflammatory in various diseases. We therefore examined sFRP5 levels in patients hospitalised for severe COVID-19 and found significant lower levels compared to healthy controls. Since sFRP5 might consequently be a molecular link for the beneficial effects of DPP4i in COVID-19, we further aimed to identify the exact source of sFRP5 in adipose tissue on cellular level. We therefore isolated pre-adipocytes, mature adipocytes and macrophages from adipose tissue biopsies and performed western-blotting. Results showed a sFRP5 expression specifically in mature adipocytes of subcutaneous and omental adipose tissue. In summary, our data suggest that DPP4i increase serum levels of anti-inflammatory sFRP5 which might be beneficial in COVID-19, reflecting a state of sFRP5 deficiency.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Anti-Inflammatory Agents ; Diabetes Mellitus, Type 2/metabolism ; Dipeptidyl-Peptidase IV Inhibitors/pharmacology ; Dipeptidyl-Peptidase IV Inhibitors/therapeutic use ; Eye Proteins/metabolism ; Humans ; Hypoglycemic Agents ; COVID-19 Drug Treatment
Chemical Substances	Adaptor Proteins, Signal Transducing ; Anti-Inflammatory Agents ; Dipeptidyl-Peptidase IV Inhibitors ; Eye Proteins ; Hypoglycemic Agents
Language	English
Publishing date	2022-09-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-18354-x
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Article ; Online: Dipeptidylpeptidase (DPP)-4 inhibitor therapy increases circulating levels of anti-inflammatory soluble frizzle receptor protein (sFRP)-5 which is decreased in severe COVID-19 disease

Juliane Brandes / Isabelle Zobel / Nathalie Rohmann / Kristina Schlicht / Corinna Geisler / Katharina Hartmann / Kathrin Türk / Witigo von Schönfels / Jan Beckmann / Florian Tran / Matthias Laudes

Scientific Reports, Vol 12, Iss 1, Pp 1-

2022 Volume 9

Abstract: ... sFRP5 in relation to DPP4 inhibition. sFRP5 is a specific antagonist to Wnt5a, a glycopeptide secreted ... Abstract Obesity and type 2 diabetes (T2D) show an increased risk for a severe COVID-19 disease ... we aimed to identify potential mechanisms for the observed DPP4i effect in COVID-19. Comparing T2D subjects ...

Abstract	Abstract Obesity and type 2 diabetes (T2D) show an increased risk for a severe COVID-19 disease. Treatment with DPP4 inhibitor (DPP4i) results in reduced mortality and better clinical outcome. Here, we aimed to identify potential mechanisms for the observed DPP4i effect in COVID-19. Comparing T2D subjects with and without DPP4i treatment, we identified a significant increase of the anti-inflammatory adipokine sFRP5 in relation to DPP4 inhibition. sFRP5 is a specific antagonist to Wnt5a, a glycopeptide secreted by adipose tissue macrophages acting pro-inflammatory in various diseases. We therefore examined sFRP5 levels in patients hospitalised for severe COVID-19 and found significant lower levels compared to healthy controls. Since sFRP5 might consequently be a molecular link for the beneficial effects of DPP4i in COVID-19, we further aimed to identify the exact source of sFRP5 in adipose tissue on cellular level. We therefore isolated pre-adipocytes, mature adipocytes and macrophages from adipose tissue biopsies and performed western-blotting. Results showed a sFRP5 expression specifically in mature adipocytes of subcutaneous and omental adipose tissue. In summary, our data suggest that DPP4i increase serum levels of anti-inflammatory sFRP5 which might be beneficial in COVID-19, reflecting a state of sFRP5 deficiency.
Keywords	Medicine ; R ; Science ; Q
Subject code	610 ; 616
Language	English
Publishing date	2022-09-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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