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Article ; Online: P2X7R: pivotal player in sepsis-induced liver damage.

Vuerich, Marta

2021 Volume 16, Issue 4, Page(s) 473–474

MeSH term(s)	Humans ; Oxidative Stress ; Purinergic P2X Receptor Antagonists ; Receptors, Purinergic P2X7 ; Sepsis
Chemical Substances	Purinergic P2X Receptor Antagonists ; Receptors, Purinergic P2X7
Language	English
Publishing date	2021-01-18
Publishing country	Netherlands
Document type	Journal Article ; Comment
ZDB-ID	2172143-9
ISSN	1573-9546 ; 1573-9538
ISSN (online)	1573-9546
ISSN	1573-9538
DOI	10.1007/s11302-020-09757-4
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Article ; Online: Transcriptome profiling of PBMCs and formalin-fixed autopsy tissues from COVID-19 patients.

Vuerich, Marta / Wang, Na / Kalbasi, Ahmadreza / Graham, Jonathon J / Longhi, Maria Serena

STAR protocols

2022 Volume 3, Issue 1, Page(s) 101156

Abstract: Here we present an optimized protocol for transcriptome profiling of COVID-19 patient samples, including peripheral blood mononuclear cells (PBMCs) and formalin-fixed paraffin-embedded tissue samples obtained from the lung, liver, heart, kidney, and ... ...

Abstract	Here we present an optimized protocol for transcriptome profiling of COVID-19 patient samples, including peripheral blood mononuclear cells (PBMCs) and formalin-fixed paraffin-embedded tissue samples obtained from the lung, liver, heart, kidney, and spleen, with the matched controls. We describe RNA extraction and subsequent transcriptome analysis using NanoString technology of the patient samples. The protocol provides information about sample preparation, RNA extraction, and NanoString profiling and analysis. It can be also applied to differentiated Th17 and Treg subsets or formalin-fixed colon tissue samples. For complete details on the use and execution of this protocol, please refer to Wang et al. (2021).
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Autopsy ; COVID-19/diagnosis ; COVID-19/genetics ; COVID-19/virology ; Case-Control Studies ; Female ; Formaldehyde/chemistry ; Humans ; Leukocytes, Mononuclear/metabolism ; Male ; Middle Aged ; RNA, Viral/analysis ; RNA, Viral/genetics ; SARS-CoV-2/genetics ; SARS-CoV-2/isolation & purification ; Tissue Fixation/methods ; Transcriptome ; Young Adult
Chemical Substances	RNA, Viral ; Formaldehyde (1HG84L3525)
Language	English
Publishing date	2022-01-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2022.101156
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Article ; Online: Ectonucleotidases in Intestinal and Hepatic Inflammation.

Vuerich, Marta / Robson, Simon C / Longhi, Maria Serena

Frontiers in immunology

2019 Volume 10, Page(s) 507

Abstract: Purinergic signaling modulates systemic and local inflammatory responses. Extracellular nucleotides, including eATP, promote inflammation, at least in part via the inflammasome upon engagement of P2 purinergic receptors. In contrast, adenosine generated ... ...

Abstract	Purinergic signaling modulates systemic and local inflammatory responses. Extracellular nucleotides, including eATP, promote inflammation, at least in part via the inflammasome upon engagement of P2 purinergic receptors. In contrast, adenosine generated during eATP phosphohydrolysis by ectonucleotidases, triggers immunosuppressive/anti-inflammatory pathways. Mounting evidence supports the role of ectonucleotidases, especially ENTPD1/CD39 and CD73, in the control of several inflammatory conditions, ranging from infectious disease, organ fibrosis to oncogenesis. Our experimental data generated over the years have indicated both CD39 and CD73 serve as pivotal regulators of intestinal and hepatic inflammation. In this context, immune cell responses are regulated by the balance between eATP and adenosine, potentially impacting disease outcomes as in gastrointestinal infection, inflammatory bowel disease, ischemia reperfusion injury of the bowel and liver, autoimmune or viral hepatitis and other inflammatory conditions, such as cancer. In this review, we report the most recent discoveries on the role of ENTPD1/CD39, CD73, and other ectonucleotidases in the regulation of intestinal and hepatic inflammation. We discuss the present knowledge, highlight the most intriguing and promising experimental data and comment on important aspects that still need to be addressed to develop purinergic-based therapies for these important illnesses.
MeSH term(s)	5'-Nucleotidase/metabolism ; Adenosine Triphosphate/metabolism ; Animals ; Apyrase/metabolism ; GPI-Linked Proteins/metabolism ; Hepatitis, Autoimmune/enzymology ; Hepatitis, Autoimmune/pathology ; Hepatitis, Viral, Human/enzymology ; Hepatitis, Viral, Human/pathology ; Humans ; Inflammatory Bowel Diseases/enzymology ; Inflammatory Bowel Diseases/pathology ; Intestines/enzymology ; Intestines/pathology ; Liver/enzymology ; Liver/pathology ; Receptors, Purinergic P2/metabolism ; Reperfusion Injury/enzymology ; Reperfusion Injury/pathology ; Signal Transduction
Chemical Substances	GPI-Linked Proteins ; Receptors, Purinergic P2 ; Adenosine Triphosphate (8L70Q75FXE) ; 5'-Nucleotidase (EC 3.1.3.5) ; NT5E protein, human (EC 3.1.3.5) ; Apyrase (EC 3.6.1.5) ; ENTPD1 protein, human (EC 3.6.1.5)
Language	English
Publishing date	2019-03-19
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.00507
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Article ; Online: Control of Gut Inflammation by Modulation of Purinergic Signaling.

Vuerich, Marta / Mukherjee, Samiran / Robson, Simon C / Longhi, Maria Serena

Frontiers in immunology

2020 Volume 11, Page(s) 1882

Abstract: Inflammatory bowel disease (IBD) is a serious inflammatory condition of the gastrointestinal tract. Crohn's disease (CD) and ulcerative colitis (UC) are two of the most common IBD manifestations and are both associated with unfettered inflammation, often ...

Abstract	Inflammatory bowel disease (IBD) is a serious inflammatory condition of the gastrointestinal tract. Crohn's disease (CD) and ulcerative colitis (UC) are two of the most common IBD manifestations and are both associated with unfettered inflammation, often refractory to conventional immunosuppressive treatment. In both conditions, imbalance between effector and regulatory cell immune responses has been documented and is thought to contribute to disease pathogenesis. Purinergic signaling is a known modulator of systemic and local inflammation and growing evidences point to extracellular ATP/adenosine imbalance as a key determinant factor in IBD-associated immune dysregulation.
MeSH term(s)	Animals ; Humans ; Inflammation/immunology ; Inflammation/metabolism ; Inflammatory Bowel Diseases/immunology ; Inflammatory Bowel Diseases/metabolism ; Purines/immunology ; Purines/metabolism ; Receptors, Purinergic P1/immunology ; Receptors, Purinergic P1/metabolism ; Receptors, Purinergic P2/immunology ; Receptors, Purinergic P2/metabolism ; Signal Transduction/immunology
Chemical Substances	Purines ; Receptors, Purinergic P1 ; Receptors, Purinergic P2
Language	English
Publishing date	2020-09-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01882
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Article ; Online: Transcriptome profiling of PBMCs and formalin-fixed autopsy tissues from COVID-19 patients

Marta Vuerich / Na Wang / Ahmadreza Kalbasi / Jonathon J. Graham / Maria Serena Longhi

STAR Protocols, Vol 3, Iss 1, Pp 101156- (2022)

2022

Abstract: Summary: Here we present an optimized protocol for transcriptome profiling of COVID-19 patient samples, including peripheral blood mononuclear cells (PBMCs) and formalin-fixed paraffin-embedded tissue samples obtained from the lung, liver, heart, kidney, ...

Abstract	Summary: Here we present an optimized protocol for transcriptome profiling of COVID-19 patient samples, including peripheral blood mononuclear cells (PBMCs) and formalin-fixed paraffin-embedded tissue samples obtained from the lung, liver, heart, kidney, and spleen, with the matched controls. We describe RNA extraction and subsequent transcriptome analysis using NanoString technology of the patient samples. The protocol provides information about sample preparation, RNA extraction, and NanoString profiling and analysis. It can be also applied to differentiated Th17 and Treg subsets or formalin-fixed colon tissue samples.For complete details on the use and execution of this protocol, please refer to Wang et al. (2021).
Keywords	Cell Biology ; Cell isolation ; Cell-based Assays ; Clinical Protocol ; Gene Expression ; Health Sciences ; Science (General) ; Q1-390
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Dysfunctional Immune Regulation in Autoimmune Hepatitis: From Pathogenesis to Novel Therapies.

Vuerich, Marta / Wang, Na / Kalbasi, Ahmadreza / Graham, Jonathon J / Longhi, Maria Serena

Frontiers in immunology

2021 Volume 12, Page(s) 746436

Abstract: Autoimmune hepatitis (AIH) is a chronic inflammatory disorder characterized by hypergammaglobulinemia, presence of serum autoantibodies and histological features of interface hepatitis. AIH therapeutic management still relies on the administration of ... ...

Abstract	Autoimmune hepatitis (AIH) is a chronic inflammatory disorder characterized by hypergammaglobulinemia, presence of serum autoantibodies and histological features of interface hepatitis. AIH therapeutic management still relies on the administration of corticosteroids, azathioprine and other immunosuppressants like calcineurin inhibitors and mycophenolate mofetil. Withdrawal of immunosuppression often results in disease relapse, and, in some cases, therapy is ineffective or associated with serious side effects. Understanding the mechanisms underlying AIH pathogenesis is therefore of paramount importance to develop more effective and well tolerated agents capable of restoring immunotolerance to liver autoantigens. Imbalance between effector and regulatory cells permits liver damage perpetuation and progression in AIH. Impaired expression and regulation of CD39, an ectoenzyme key to immunotolerance maintenance, have been reported in Tregs and effector Th17-cells derived from AIH patients. Interference with these altered immunoregulatory pathways may open new therapeutic avenues that, in addition to limiting aberrant inflammatory responses, would also reconstitute immune homeostasis. In this review, we highlight the most recent findings in AIH immunopathogenesis and discuss how these could inform and direct the development of novel therapeutic tools.
MeSH term(s)	Animals ; Hepatitis, Autoimmune/drug therapy ; Hepatitis, Autoimmune/immunology ; Humans
Language	English
Publishing date	2021-09-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.746436
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Article: Metabolic Switch in the Tumor Microenvironment Determines Immune Responses to Anti-cancer Therapy.

Wegiel, Barbara / Vuerich, Marta / Daneshmandi, Saeed / Seth, Pankaj

Frontiers in oncology

2018 Volume 8, Page(s) 284

Abstract: Tumor-induced immune tolerance permits growth and spread of malignant cells. Cancer cells have strong influence on surrounding cells and shape the hypoxic tumor microenvironment (TME) facilitating cancer progression. A dynamic change in glucose ... ...

Abstract	Tumor-induced immune tolerance permits growth and spread of malignant cells. Cancer cells have strong influence on surrounding cells and shape the hypoxic tumor microenvironment (TME) facilitating cancer progression. A dynamic change in glucose metabolism occurring in cancer cells and its influence on the TME are still poorly understood. Indeed, cancer and/or immune cells undergo rapid adaptation in metabolic pathways during cancer progression. Metabolic reprograming affects macrophages, T cells, and myeloid derived suppressor cells (MDSCs) among other immune cells. Their role in the TME depends on a nature and concentration of factors, such as cytokines, reactive oxygen species (ROS), growth factors, and most importantly, diffusible metabolites (i.e., lactate). Further, the amounts of available nutrients and oxygen as well as activity of microbiota may influence metabolic pathways in the TME. The roles of metabolites in regulating of the interaction between immune and cancer cell are highlighted in this review. Targeting metabolic reprogramming or signaling pathways controlling cell metabolism in the TME might be a potential strategy for anti-cancer therapy alone or in combination with current immunotherapies.
Language	English
Publishing date	2018-08-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2018.00284
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Article ; Online: Purinergic signaling in the immune system.

Di Virgilio, Francesco / Vuerich, Marta

Autonomic neuroscience : basic & clinical

2015 Volume 191, Page(s) 117–123

Abstract: Extracellular ATP and its metabolite adenosine are increasingly recognized as key mediators of the immune response. Depending on the concentration, ATP may act as an immunostimulant or an immunodepressant, while adenosine is generally acknowledged to be ... ...

Abstract	Extracellular ATP and its metabolite adenosine are increasingly recognized as key mediators of the immune response. Depending on the concentration, ATP may act as an immunostimulant or an immunodepressant, while adenosine is generally acknowledged to be a potent immunosupressor molecule. Signals delivered by extracellular ATP and adenosine are detected and transduced by P2 and P1 receptors, respectively. Virtually all immune cells express P2 and P1 receptors, thus purinergic signaling affects all aspects of immunity and inflammation. This realization has prompted a burst of novel investigations aimed at the design and synthesis of P2- or P1-targeted drugs for the treatment of chronic inflammatory diseases and cancer. In this review we will summarize the most recent developments in this field.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Humans ; Immune System/metabolism ; Receptors, Purinergic/metabolism
Chemical Substances	Receptors, Purinergic ; Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2015-04-30
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2020105-9
ISSN	1872-7484 ; 1566-0702
ISSN (online)	1872-7484
ISSN	1566-0702
DOI	10.1016/j.autneu.2015.04.011
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Article ; Online: Dysregulation of Adenosinergic Signaling in Systemic and Organ-Specific Autoimmunity.

Vuerich, Marta / Harshe, Rasika P / Robson, Simon C / Longhi, Maria Serena

International journal of molecular sciences

2019 Volume 20, Issue 3

Abstract: Exact causes for autoimmune diseases remain unclear and no cures are available. Breakdown of immunotolerance could set the stage for unfettered immune responses that target self-antigens. Impaired regulatory immune mechanisms could have permissive roles ... ...

Abstract	Exact causes for autoimmune diseases remain unclear and no cures are available. Breakdown of immunotolerance could set the stage for unfettered immune responses that target self-antigens. Impaired regulatory immune mechanisms could have permissive roles in autoreactivity. Abnormal regulatory immune cell function, therefore, might be a major determinant of the pathogenesis of autoimmune disease. All current treatments are associated with some level of clinical toxicity. Treatment to specifically target dysregulated immunity in these diseases would be a great advance. Extracellular adenosine is a signaling mediator that suppresses inflammation through activation of P1 receptors, most active under pathological conditions. Mounting evidence has linked alterations in the generation of adenosine from extracellular nucleotides by ectonucleotidases, and associated perturbations in purinergic signaling, to the immunological disruption and loss of immunotolerance in autoimmunity. Targeted modulation of the purinergic signaling by either targeting ectonucleotidases or modulating P1 purinergic receptors could therefore restore the balance between autoreactive immune responses; and thereby allow reestablishment of immunotolerance. We review the roles of CD39 and CD73 ectoenzymes in inflammatory states and with the dysregulation of P1 receptor signaling in systemic and organ-specific autoimmunity. Correction of such perturbations could be exploited in potential therapeutic applications.
MeSH term(s)	Adenosine/metabolism ; Antigens, Neoplasm/metabolism ; Apyrase/metabolism ; Autoimmune Diseases/drug therapy ; Autoimmune Diseases/metabolism ; Humans ; Organ Specificity ; Receptors, Purinergic P1/metabolism ; Signal Transduction ; Tetraspanins/metabolism
Chemical Substances	Antigens, Neoplasm ; CD37 protein, human ; Receptors, Purinergic P1 ; Tetraspanins ; Apyrase (EC 3.6.1.5) ; ENTPD1 protein, human (EC 3.6.1.5) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2019-01-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20030528
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Article ; Online: Blockade of PGK1 and ALDOA enhances bilirubin control of Th17 cells in Crohn's disease.

Vuerich, Marta / Wang, Na / Graham, Jonathon J / Gao, Li / Zhang, Wei / Kalbasi, Ahmadreza / Zhang, Lina / Csizmadia, Eva / Hristopoulos, Jason / Ma, Yun / Kokkotou, Efi / Cheifetz, Adam S / Robson, Simon C / Longhi, Maria Serena

Communications biology

2022 Volume 5, Issue 1, Page(s) 994

Abstract: Unconjugated bilirubin (UCB) confers Th17-cells immunosuppressive features by activating aryl-hydrocarbon-receptor, a modulator of toxin and adaptive immune responses. In Crohn's disease, Th17-cells fail to acquire regulatory properties in response to ... ...

Abstract	Unconjugated bilirubin (UCB) confers Th17-cells immunosuppressive features by activating aryl-hydrocarbon-receptor, a modulator of toxin and adaptive immune responses. In Crohn's disease, Th17-cells fail to acquire regulatory properties in response to UCB, remaining at an inflammatory/pathogenic state. Here we show that UCB modulates Th17-cell metabolism by limiting glycolysis and through downregulation of glycolysis-related genes, namely phosphoglycerate-kinase-1 (PGK1) and aldolase-A (ALDOA). Th17-cells of Crohn's disease patients display heightened PGK1 and ALDOA and defective response to UCB. Silencing of PGK1 or ALDOA restores Th17-cell response to UCB, as reflected by increase in immunoregulatory markers like FOXP3, IL-10 and CD39. In vivo, PGK1 and ALDOA silencing enhances UCB salutary effects in trinitro-benzene-sulfonic-acid-induced colitis in NOD/scid/gamma humanized mice where control over disease activity and enhanced immunoregulatory phenotypes are achieved. PGK1 and/or ALDOA blockade might have therapeutic effects in Crohn's disease by favoring acquisition of regulatory properties by Th17-cells along with control over their pathogenic potential.
MeSH term(s)	Animals ; Benzene/metabolism ; Bilirubin ; Crohn Disease/genetics ; Forkhead Transcription Factors/metabolism ; Fructose-Bisphosphate Aldolase/metabolism ; Humans ; Interleukin-10/metabolism ; Mice ; Mice, Inbred NOD ; Phosphoglycerate Kinase/antagonists & inhibitors ; Th17 Cells
Chemical Substances	Forkhead Transcription Factors ; Interleukin-10 (130068-27-8) ; Phosphoglycerate Kinase (EC 2.7.2.3) ; Fructose-Bisphosphate Aldolase (EC 4.1.2.13) ; Benzene (J64922108F) ; Bilirubin (RFM9X3LJ49)
Language	English
Publishing date	2022-09-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-022-03913-9
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