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Article ; Online: Interplay between hypoxia and inflammation contributes to the progression and severity of respiratory viral diseases.

Bhattacharya, Sulagna / Agarwal, Sakshi / Shrimali, Nishith M / Guchhait, Prasenjit

2021 Volume 81, Page(s) 101000

Abstract: History of pandemics is dominated by viral infections and specifically respiratory viral diseases like influenza and COVID-19. Lower respiratory tract infection is the fourth leading cause of death worldwide. Crosstalk between resultant inflammation and ... ...

Abstract	History of pandemics is dominated by viral infections and specifically respiratory viral diseases like influenza and COVID-19. Lower respiratory tract infection is the fourth leading cause of death worldwide. Crosstalk between resultant inflammation and hypoxic microenvironment may impair ventilatory response of lungs. This reduces arterial partial pressure of oxygen, termed as hypoxemia, which is observed in a section of patients with respiratory virus infections including SARS-CoV-2 (COVID-19). In this review, we describe the interplay between inflammation and hypoxic microenvironment in respiratory viral infection and its contribution to disease pathogenesis.
MeSH term(s)	COVID-19 ; Humans ; Hypoxia ; Inflammation ; Pandemics ; SARS-CoV-2
Language	English
Publishing date	2021-07-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	197640-0
ISSN	1872-9452 ; 0098-2997
ISSN (online)	1872-9452
ISSN	0098-2997
DOI	10.1016/j.mam.2021.101000
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Article ; Online: Gain-of-function Tibetan PHD2

Bhattacharya, Sulagna / Shrimali, Nishith M / Mohammad, Ghulam / Koul, Parvaiz A / Prchal, Josef T / Guchhait, Prasenjit

EBioMedicine

2021 Volume 68, Page(s) 103418

Abstract: Background: We have previously described an evolutionarily selected Tibetan prolyl hydroxylase-2 (PHD2: Methods: We genotyped the Tibetans using DNA isolated from whole blood. Thereafter immunophenotying was performed on PBMCs from homozygous PHD2: ...

Abstract	Background: We have previously described an evolutionarily selected Tibetan prolyl hydroxylase-2 (PHD2 Methods: We genotyped the Tibetans using DNA isolated from whole blood. Thereafter immunophenotying was performed on PBMCs from homozygous PHD2 Findings: We report that homozygous PHD2 Interpretation: Our report suggests that gain-of-function PHD2 Funding: This study is supported by the Department of Biotechnology, Government of India.
MeSH term(s)	Adult ; Altitude Sickness/chemically induced ; Altitude Sickness/genetics ; Altitude Sickness/prevention & control ; Animals ; Case-Control Studies ; Disease Models, Animal ; Female ; Gain of Function Mutation ; Humans ; Hypertension, Pulmonary/chemically induced ; Hypertension, Pulmonary/genetics ; Hypertension, Pulmonary/prevention & control ; Hypoxia-Inducible Factor-Proline Dioxygenases/genetics ; Immunophenotyping ; Ketoglutaric Acids/adverse effects ; Male ; Mice ; Travel ; U937 Cells ; Young Adult
Chemical Substances	Ketoglutaric Acids ; EGLN1 protein, human (EC 1.14.11.2) ; Hypoxia-Inducible Factor-Proline Dioxygenases (EC 1.14.11.29)
Language	English
Publishing date	2021-06-05
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2021.103418
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Article ; Online: Dietary alpha-ketoglutarate inhibits SARS CoV-2 infection and rescues inflamed lungs to restore O

Agarwal, Sakshi / Kaur, Simrandeep / Asuru, Tejeswara Rao / Joshi, Garima / Shrimali, Nishith M / Singh, Anamika / Singh, Oinam Ningthemmani / Srivastva, Puneet / Shrivastava, Tripti / Vrati, Sudhanshu / Surjit, Milan / Guchhait, Prasenjit

Clinical and translational medicine

2022 Volume 12, Issue 9, Page(s) e1041

MeSH term(s)	COVID-19 ; Humans ; Ketoglutaric Acids/pharmacology ; Lung ; Severe Acute Respiratory Syndrome ; Virus Replication
Chemical Substances	Ketoglutaric Acids
Language	English
Publishing date	2022-09-19
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2697013-2
ISSN	2001-1326 ; 2001-1326
ISSN (online)	2001-1326
ISSN	2001-1326
DOI	10.1002/ctm2.1041
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Article ; Online: Inhibition of cellular activation induced by platelet factor 4 via the CXCR3 pathway ameliorates Japanese encephalitis and dengue viral infections.

Singh, Anamika / Ghosh, Riya / Asuru, Tejeswara Rao / Prajapat, Surendra K / Joshi, Garima / Gaur, Kishan K / Shrimali, Nishith M / Ojha, Amrita / Vikram, Naval K / Poncz, Mortimer / Kalia, Manjula / Guchhait, Prasenjit

Journal of thrombosis and haemostasis : JTH

2023 Volume 22, Issue 3, Page(s) 818–833

Abstract: Background: Activated platelets secrete platelet factor 4 (PF4), which contributes to viral pathogenesis. Recently, we reported the proviral role of PF4 in replication of closely related flaviviruses, Japanese encephalitis virus (JEV) and dengue virus ( ... ...

Abstract	Background: Activated platelets secrete platelet factor 4 (PF4), which contributes to viral pathogenesis. Recently, we reported the proviral role of PF4 in replication of closely related flaviviruses, Japanese encephalitis virus (JEV) and dengue virus (DENV). Objectives: This study aimed to investigate the detailed mechanism of PF4-mediated virus replication. Methods: PF4 Results: PF4 Conclusion: These studies suggest that PF4 deficiency or inhibition of the PF4:CXCR3 pathway prevents JEV and DENV infection. The studies also highlight the PF4:CXCR3 axis as a potential target to develop treatment regimens against flaviviruses.
MeSH term(s)	Animals ; Humans ; Mice ; Acetamides ; Dengue/drug therapy ; Dengue/metabolism ; Encephalitis Virus, Japanese/physiology ; Encephalitis, Japanese/drug therapy ; Immunologic Factors ; Platelet Factor 4 ; Pyrimidinones ; Receptors, CXCR3
Chemical Substances	Acetamides ; CXCR3 protein, human ; Immunologic Factors ; N-(1-(3-(4-ethoxyphenyl)-4-oxo-3,4-dihydropyrido(2,3-d)pyrimidin-2-yl)ethyl)-N-pyridin-3-ylmethyl-2-(4-trifluoromethoxyphenyl)acetamide ; Platelet Factor 4 (37270-94-3) ; Pyrimidinones ; Receptors, CXCR3 ; Pf4 protein, mouse
Language	English
Publishing date	2023-11-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2112661-6
ISSN	1538-7836 ; 1538-7933
ISSN (online)	1538-7836
ISSN	1538-7933
DOI	10.1016/j.jtha.2023.11.015
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Zs.A 5805: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: α-Ketoglutarate Inhibits Thrombosis and Inflammation by Prolyl Hydroxylase-2 Mediated Inactivation of Phospho-Akt.

Shrimali, Nishith M / Agarwal, Sakshi / Kaur, Simrandeep / Bhattacharya, Sulagna / Bhattacharyya, Sankar / Prchal, Josef T / Guchhait, Prasenjit

EBioMedicine

2021 Volume 73, Page(s) 103672

Abstract: Background: Phospho-Akt1 (pAkt1) undergoes prolyl hydroxylation at Pro125 and Pro313 by the prolyl hydroxylase-2 (PHD2) in a reaction decarboxylating α-ketoglutarate (αKG). We investigated whether the αKG supplementation could inhibit Akt-mediated ... ...

Abstract	Background: Phospho-Akt1 (pAkt1) undergoes prolyl hydroxylation at Pro125 and Pro313 by the prolyl hydroxylase-2 (PHD2) in a reaction decarboxylating α-ketoglutarate (αKG). We investigated whether the αKG supplementation could inhibit Akt-mediated activation of platelets and monocytes, in vitro as well as in vivo, by augmenting PHD2 activity. Methods: We treated platelets or monocytes isolated from healthy individuals with αKG in presence of agonists in vitro and assessed the signalling molecules including pAkt1. We supplemented mice with dietary αKG and estimated the functional responses of platelets and monocytes ex vivo. Further, we investigated the impact of dietary αKG on inflammation and thrombosis in lungs of mice either treated with thrombosis-inducing agent carrageenan or infected with SARS-CoV-2. Findings: Octyl αKG supplementation to platelets promoted PHD2 activity through elevated intracellular αKG to succinate ratio, and reduced aggregation in vitro by suppressing pAkt1(Thr308). Augmented PHD2 activity was confirmed by increased hydroxylated-proline and enhanced binding of PHD2 to pAkt in αKG-treated platelets. Contrastingly, inhibitors of PHD2 significantly increased pAkt1 in platelets. Octyl-αKG followed similar mechanism in monocytes to inhibit cytokine secretion in vitro. Our data also describe a suppressed pAkt1 and reduced activation of platelets and leukocytes ex vivo from mice supplemented with dietary αKG, unaccompanied by alteration in their number. Dietary αKG significantly reduced clot formation and leukocyte accumulation in various organs including lungs of mice treated with thrombosis-inducing agent carrageenan. Importantly, in SARS-CoV-2 infected hamsters, we observed a significant rescue effect of dietary αKG on inflamed lungs with significantly reduced leukocyte accumulation, clot formation and viral load alongside down-modulation of pAkt in the lung of the infected animals. Interpretation: Our study suggests that dietary αKG supplementation prevents Akt-driven maladies such as thrombosis and inflammation and rescues pathology of COVID19-infected lungs. Funding: Study was funded by the Department of Biotechnology (DBT), Govt. of India (grants: BT/PR22881 and BT/PR22985); and the Science and Engineering Research Board, Govt. of India (CRG/000092).
MeSH term(s)	Animals ; Blood Platelets/cytology ; Blood Platelets/drug effects ; Blood Platelets/metabolism ; COVID-19/pathology ; COVID-19/prevention & control ; COVID-19/veterinary ; COVID-19/virology ; Cricetinae ; Dietary Supplements ; Down-Regulation/drug effects ; Humans ; Ketoglutaric Acids/pharmacology ; Ketoglutaric Acids/therapeutic use ; Lung/metabolism ; Lung/pathology ; Mesocricetus ; Mice ; Mice, Inbred BALB C ; Monocytes/cytology ; Monocytes/drug effects ; Monocytes/metabolism ; Phosphorylation ; Platelet Aggregation/drug effects ; Prolyl Hydroxylases/metabolism ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; SARS-CoV-2/isolation & purification ; SARS-CoV-2/physiology ; Thrombosis/chemically induced ; Thrombosis/pathology ; Thrombosis/prevention & control ; Thrombosis/veterinary
Chemical Substances	Ketoglutaric Acids ; Protein Isoforms ; Prolyl Hydroxylases (EC 1.14.11.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2021-11-02
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2021.103672
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Zs.A 7090: Show issues

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Article ; Online: α-Ketoglutarate Inhibits Thrombosis and Inflammation by Prolyl Hydroxylase-2 Mediated Inactivation of Phospho-Akt

Nishith M Shrimali / Sakshi Agarwal / Simrandeep Kaur / Sulagna Bhattacharya / Sankar Bhattacharyya / Josef T Prchal / Prasenjit Guchhait

EBioMedicine, Vol 73, Iss , Pp 103672- (2021)

2021

Abstract	Background: Phospho-Akt1 (pAkt1) undergoes prolyl hydroxylation at Pro125 and Pro313 by the prolyl hydroxylase-2 (PHD2) in a reaction decarboxylating α-ketoglutarate (αKG). We investigated whether the αKG supplementation could inhibit Akt-mediated activation of platelets and monocytes, in vitro as well as in vivo, by augmenting PHD2 activity. Methods: We treated platelets or monocytes isolated from healthy individuals with αKG in presence of agonists in vitro and assessed the signalling molecules including pAkt1. We supplemented mice with dietary αKG and estimated the functional responses of platelets and monocytes ex vivo. Further, we investigated the impact of dietary αKG on inflammation and thrombosis in lungs of mice either treated with thrombosis-inducing agent carrageenan or infected with SARS-CoV-2. Findings: Octyl αKG supplementation to platelets promoted PHD2 activity through elevated intracellular αKG to succinate ratio, and reduced aggregation in vitro by suppressing pAkt1(Thr308). Augmented PHD2 activity was confirmed by increased hydroxylated-proline and enhanced binding of PHD2 to pAkt in αKG-treated platelets. Contrastingly, inhibitors of PHD2 significantly increased pAkt1 in platelets. Octyl-αKG followed similar mechanism in monocytes to inhibit cytokine secretion in vitro. Our data also describe a suppressed pAkt1 and reduced activation of platelets and leukocytes ex vivo from mice supplemented with dietary αKG, unaccompanied by alteration in their number. Dietary αKG significantly reduced clot formation and leukocyte accumulation in various organs including lungs of mice treated with thrombosis-inducing agent carrageenan. Importantly, in SARS-CoV-2 infected hamsters, we observed a significant rescue effect of dietary αKG on inflamed lungs with significantly reduced leukocyte accumulation, clot formation and viral load alongside down-modulation of pAkt in the lung of the infected animals. Interpretation: Our study suggests that dietary αKG supplementation prevents Akt-driven maladies such as thrombosis and inflammation and rescues pathology of COVID19-infected lungs. Funding: Study was funded by the Department of Biotechnology (DBT), Govt. of India (grants: BT/PR22881 and BT/PR22985); and the Science and Engineering Research Board, Govt. of India (CRG/000092).
Keywords	αKG ; PHD2 ; Akt ; thrombosis ; inflammation ; SARS-CoV-2 ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	570
Language	English
Publishing date	2021-11-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Gain-of-function Tibetan PHD2D4E;C127S variant suppresses monocyte function

Sulagna Bhattacharya / Nishith M Shrimali / Ghulam Mohammad / Parvaiz A Koul / Josef T Prchal / Prasenjit Guchhait

EBioMedicine, Vol 68, Iss , Pp 103418- (2021)

A lesson in inflammatory response to inspired hypoxia

2021

Abstract: Background: We have previously described an evolutionarily selected Tibetan prolyl hydroxylase-2 (PHD2D4E;C127S) variant that degrades the hypoxia-inducible factor (HIFα) more efficiently and protects these highlanders from hypoxia-triggered elevation in ...

Abstract	Background: We have previously described an evolutionarily selected Tibetan prolyl hydroxylase-2 (PHD2D4E;C127S) variant that degrades the hypoxia-inducible factor (HIFα) more efficiently and protects these highlanders from hypoxia-triggered elevation in haemoglobin concentration. High altitude is known to cause acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) in a section of rapidly ascending non-acclimatised lowlanders. These morbidities are often accompanied by inflammatory response and exposure to hypobaric hypoxia is presumed to be the principal causative agent. We have investigated whether PHD2D4E;C127S variant is associated with prevention of hypoxia-mediated inflammatory milieu in Tibetan highlanders and therefore identify a potential target to regulate inflammation. Methods: We genotyped the Tibetans using DNA isolated from whole blood. Thereafter immunophenotying was performed on PBMCs from homozygous PHD2D4E;C127S and PHD2WT individuals using flow cytometry. RNA isolated from these individuals was used to evaluate the peripheral level of important transcripts associated with immune as well as hypoxia response employing the nCounter technology. The ex-vivo findings were validated by generating monocytic cell lines (U937 cell line) expressing PHD2D4E;C127S and PHD2WT variants post depletion of endogenous PHD2. We had also collected whole blood samples from healthy travellers and travellers afflicted with AMS and HAPE to evaluate the significance of our ex-vivo and in vitro findings. Hereafter, we also attempted to resolve hypoxia-triggered inflammation in vitro as well as in vivo by augmenting the function of PHD2 using alpha-ketoglutarate (αKG), a co-factor of PHD2. Findings: We report that homozygous PHD2D4E;C127S highlanders harbour less inflammatory and patrolling monocytes in circulation as compared to Tibetan PHD2WT highlanders. In response to in vitro hypoxia, secretion of IL6 and IL1β from PHD2D4E;C127S monocytes, and their chemotactic response compared to the PHD2WT are ...
Keywords	High altitude hypoxia ; Tibetan ; PHD2 variant ; HAPE ; Monocyte ; Inflammation ; Medicine ; R ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Dietary αKG inhibits SARS CoV-2 infection and rescues inflamed lungs to restore normal O2 saturation in animals

Agarwal, Sakshi / Kaur, Simrandeep / Asuru, Tejeswara Rao / Joshi, Garima / Shrimali, Nishith M / Singh, Anamika / Singh, Oinam N / Srivastva, Puneet / Shrivastava, Tripti / Vrati, Sudhanshu / Surjit, Milan / Guchhait, Prasenjit

bioRxiv

Abstract: Our recent works described the rescue effect of α-ketoglutarate (αKG, a metabolite of Krebs cycle) on thrombosis and inflammation in animals. αKG augments activity of prolyl hydroxylase 2 (PHD2), which in turn degrades proline residues of substrates like ...

Abstract	Our recent works described the rescue effect of α-ketoglutarate (αKG, a metabolite of Krebs cycle) on thrombosis and inflammation in animals. αKG augments activity of prolyl hydroxylase 2 (PHD2), which in turn degrades proline residues of substrates like phosphorylated Akt (pAkt) and hypoxia inducible factor (HIF)α. Here we describe the inhibitory effect of octyl αKG on pAkt as well as on HIF1α/HIF2α, and in turn decreasing SARS CoV-2 replication in Vero E6 cells. αKG failed to inhibit the viral replication and Akt phosphorylation in PHD2-knockdown U937 cells transiently expressing ACE2. Contrastingly, triciribine (TCN, an Akt-inhibitor) inhibited viral replication alongside a downmodulation of pAkt in PHD2-KD cells. Dietary αKG significantly inhibited viral infection and rescued hamsters from thrombus formation and inflammation in lungs, the known causes of acute respiratory distress syndrome (ARDS) in COVID-19. αKG supplementation also reduced the apoptotic death of lung tissues in infected animals, alongside a downmodulation of pAkt and HIF2α. αKG supplementation neither affected IgG levels against SARS CoV-2 RBD protein nor altered the neutralization antibody response against SARS CoV-2. It did not interfere with the percentage of interferon-γ positive (IFNγ+) CD4+ and IFNγ+CD8+ T cells in infected animals. The extended work in balb/c mice transiently expressing ACE2 showed a similar effect of αKG in reducing accumulation of inflammatory immune cells and cytokines, including IL6, IL1β and TNFα, in lungs as well as in circulation of infected animals. Pro-thrombotic markers like platelet microparticles and platelet-leukocyte aggregates were reduced significantly in infected mice after αKG supplementation. Importantly, αKG supplementation restored the O2 saturation (SpO2) in circulation of SARS CoV-2 infected hamsters and mice, suggesting a potential therapeutic role of this metabolite in COVID-19 treatment.
Keywords	covid19
Language	English
Publishing date	2022-04-03
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.04.02.486853
Database	COVID19

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Article ; Online: Interplay between hypoxia and inflammation contributes to the progression and severity of respiratory viral diseases.

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Article ; Online: Gain-of-function Tibetan PHD2

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Article ; Online: Dietary alpha-ketoglutarate inhibits SARS CoV-2 infection and rescues inflamed lungs to restore O

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Article ; Online: Inhibition of cellular activation induced by platelet factor 4 via the CXCR3 pathway ameliorates Japanese encephalitis and dengue viral infections.

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Article ; Online: α-Ketoglutarate Inhibits Thrombosis and Inflammation by Prolyl Hydroxylase-2 Mediated Inactivation of Phospho-Akt.

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Article ; Online: α-Ketoglutarate Inhibits Thrombosis and Inflammation by Prolyl Hydroxylase-2 Mediated Inactivation of Phospho-Akt

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Article ; Online: Gain-of-function Tibetan PHD2D4E;C127S variant suppresses monocyte function

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Article ; Online: Dietary αKG inhibits SARS CoV-2 infection and rescues inflamed lungs to restore normal O2 saturation in animals

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