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Article ; Online: IL-6: Relevance for immunopathology of SARS-CoV-2.

Gubernatorova, E O / Gorshkova, E A / Polinova, A I / Drutskaya, M S

2020 Volume 53, Page(s) 13–24

Abstract: COVID-19 mortality is strongly associated with the development of severe pneumonia and acute respiratory distress syndrome with the worst outcome resulting in cytokine release syndrome and multiorgan failure. It is becoming critically important to ... ...

Abstract	COVID-19 mortality is strongly associated with the development of severe pneumonia and acute respiratory distress syndrome with the worst outcome resulting in cytokine release syndrome and multiorgan failure. It is becoming critically important to identify at the early stage of the infection those patients who are prone to develop the most adverse effects. Elevated systemic interleukin-6 levels in patients with COVID-19 are considered as a relevant parameter in predicting most severe course of disease and the need for intensive care. This review discusses the mechanisms by which IL-6 may possibly contribute to disease exacerbation and the potential of therapeutic approaches based on anti-IL-6 biologics.
MeSH term(s)	Antibodies, Monoclonal, Humanized/therapeutic use ; Betacoronavirus/drug effects ; Betacoronavirus/immunology ; Betacoronavirus/pathogenicity ; COVID-19 ; Coronavirus Infections/drug therapy ; Coronavirus Infections/mortality ; Coronavirus Infections/pathology ; Cytokine Release Syndrome/drug therapy ; Cytokine Release Syndrome/pathology ; Cytokine Release Syndrome/virology ; Humans ; Interleukin-6/antagonists & inhibitors ; Interleukin-6/blood ; Interleukin-6/immunology ; Lung Diseases/immunology ; Lung Diseases/pathology ; Lung Diseases/virology ; Pandemics ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/mortality ; Pneumonia, Viral/pathology ; SARS-CoV-2
Chemical Substances	Antibodies, Monoclonal, Humanized ; IL6 protein, human ; Interleukin-6 ; sarilumab (NU90V55F8I)
Keywords	covid19
Language	English
Publishing date	2020-05-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1330534-7
ISSN	1879-0305 ; 1359-6101
ISSN (online)	1879-0305
ISSN	1359-6101
DOI	10.1016/j.cytogfr.2020.05.009
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Article ; Online: Tumor Necrosis Factor and Lymphotoxin in Regulation of Intestinal Inflammation.

Gubernatorova, E O / Tumanov, A V

Biochemistry. Biokhimiia

2016 Volume 81, Issue 11, Page(s) 1309–1325

Abstract: Ulcerative colitis and Crohn's disease are the major forms of inflammatory bowel disease. Cytokines of the tumor necrosis factor (TNF) family play an important role in the regulation of intestinal inflammation. In this review, we discuss the function of ... ...

Abstract	Ulcerative colitis and Crohn's disease are the major forms of inflammatory bowel disease. Cytokines of the tumor necrosis factor (TNF) family play an important role in the regulation of intestinal inflammation. In this review, we discuss the function of key cytokines of this family - TNF and lymphotoxin (LT) - in mucosal healing, IgA production, and in control of innate lymphoid cells (ILCs), novel regulators of mucosal homeostasis in the gut. TNF plays a central role in the pathogenesis of inflammatory bowel diseases (IBD). LT regulates group 3 of ILCs and IL-22 production and protects the epithelium against damage by chemicals and mucosal bacterial pathogens. In addition, we discuss major mouse models employed to study the mechanism of intestinal inflammation, their advantages and limitations, as well as application of TNF blockers in the therapy for IBD.
MeSH term(s)	Animals ; Colitis, Ulcerative/immunology ; Colitis, Ulcerative/pathology ; Crohn Disease/immunology ; Crohn Disease/pathology ; Humans ; Interleukins/immunology ; Intestinal Mucosa/immunology ; Intestinal Mucosa/pathology ; Lymphotoxin-alpha/immunology ; Mice ; Tumor Necrosis Factor-alpha/immunology ; Interleukin-22
Chemical Substances	Interleukins ; Lymphotoxin-alpha ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2016-12-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1109-5
ISSN	1608-3040 ; 0006-2979 ; 0320-9717
ISSN (online)	1608-3040
ISSN	0006-2979 ; 0320-9717
DOI	10.1134/S0006297916110092
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Article: [Humanized Mouse Models as a Tool to Study Proinflammatory Cytokine Overexpression].

Gorshkova, E A / Zvartsev, R V / Drutskaya, M S / Gubernatorova, E O

Molekuliarnaia biologiia

2019 Volume 53, Issue 5, Page(s) 755–773

Abstract: Dysregulated proinflammatory cytokine expression may result in the development of severe pathologies, such as rheumatoid arthritis, psoriasis, and neurodegenerative diseases. Transgenic mice and, in particular, those with controllable systemic ... ...

Abstract	Dysregulated proinflammatory cytokine expression may result in the development of severe pathologies, such as rheumatoid arthritis, psoriasis, and neurodegenerative diseases. Transgenic mice and, in particular, those with controllable systemic overexpression of proinflammatory cytokines have recently become an essential instrument to study the molecular mechanisms underlying disease development. Importantly, many of the models are humanized by introducing a human cytokine gene, while leaving or removing the respective endogenous mouse gene. Humanized mice are especially valuable for biomedical research as they provide a relevant model to develop therapies based on blocking the pathogenic activity of a cytokine or to establish the functional significance of genome polymorphisms. The review discusses the available humanized mouse models with overexpression of key proinflammatory cytokines (TNF, IL-ip, and IL-6) and inflammatory cytokines with more specific functions (IL-8, IL-17, and IL-32) and their significance for basic and clinical research.
MeSH term(s)	Animals ; Arthritis, Rheumatoid/genetics ; Cytokines/biosynthesis ; Cytokines/genetics ; Cytokines/metabolism ; Disease Models, Animal ; Humans ; Inflammation Mediators/metabolism ; Mice ; Mice, Transgenic ; Neurodegenerative Diseases/genetics ; Psoriasis/genetics ; Up-Regulation
Chemical Substances	Cytokines ; Inflammation Mediators
Language	Russian
Publishing date	2019-09-18
Publishing country	Russia (Federation)
Document type	Journal Article ; Review
ZDB-ID	213542-5
ISSN	0026-8984
ISSN	0026-8984
DOI	10.1134/S0026898419050070
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Article ; Online: IL-6

Gubernatorova, E.O. / Gorshkova, E.A. / Polinova, A.I. / Drutskaya, M.S.

Cytokine & Growth Factor Reviews

Relevance for immunopathology of SARS-CoV-2

2020 Volume 53, Page(s) 13–24

Keywords	Immunology ; General Biochemistry, Genetics and Molecular Biology ; Immunology and Allergy ; Endocrinology, Diabetes and Metabolism ; covid19
Language	English
Publisher	Elsevier BV
Publishing country	us
Document type	Article ; Online
ZDB-ID	1330534-7
ISSN	1359-6101
ISSN	1359-6101
DOI	10.1016/j.cytogfr.2020.05.009
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: IL-6: Relevance for immunopathology of SARS-CoV-2

Gubernatorova, E O / Gorshkova, E A / Polinova, A I / Drutskaya, M S

Cytokine Growth Factor Rev

Abstract	COVID-19 mortality is strongly associated with the development of severe pneumonia and acute respiratory distress syndrome with the worst outcome resulting in cytokine release syndrome and multiorgan failure. It is becoming critically important to identify at the early stage of the infection those patients who are prone to develop the most adverse effects. Elevated systemic interleukin-6 levels in patients with COVID-19 are considered as a relevant parameter in predicting most severe course of disease and the need for intensive care. This review discusses the mechanisms by which IL-6 may possibly contribute to disease exacerbation and the potential of therapeutic approaches based on anti-IL-6 biologics.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #324437
Database	COVID19

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Article: [Proinflammatory and Immunoregulatory Functions of Interleukin 6 as Identified by Reverse Genetics].

Drutskaya, M S / Gogoleva, V S / Atretkhany, K-S N / Gubernatorova, E O / Zvartsev, R V / Nosenko, M A / Nedospasov, S A

Molekuliarnaia biologiia

2019 Volume 52, Issue 6, Page(s) 963–974

Abstract: Reverse genetics approach, involving genome editing, makes it possible not only to establish the nonredundant and unique functions of genes and their products, but also to construct animal models for biomedical research. Interleukin 6 (IL-6) is an ... ...

Abstract	Reverse genetics approach, involving genome editing, makes it possible not only to establish the nonredundant and unique functions of genes and their products, but also to construct animal models for biomedical research. Interleukin 6 (IL-6) is an important immunoregulatory and proinflammatory cytokine that differs from many related proteins in having a rather complicated signal transduction scheme. Apart from the multiple functions of IL-6, the most relevant biological problem of recent years was establishing what cells produce IL-6, in what form IL-6 is produced, what cells are recipients of the IL-6 signal, and what are the downstream events and physiological consequences of the IL-6 signaling cascade. Because IL-6 is involved in the pathogenesis of many diseases and is a drug target, understanding the mechanisms of its normal and pathogenic effects is important for the clinics. The review summarizes the recent data available in the field.
MeSH term(s)	Animals ; Humans ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Reverse Genetics ; Signal Transduction
Chemical Substances	Interleukin-6
Language	Russian
Publishing date	2019-01-11
Publishing country	Russia (Federation)
Document type	Journal Article ; Review
ZDB-ID	213542-5
ISSN	0026-8984
ISSN	0026-8984
DOI	10.1134/S0026898418060058
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Article ; Online: Murine Model of Intestinal Ischemia-reperfusion Injury.

Gubernatorova, Ekaterina O / Perez-Chanona, Ernesto / Koroleva, Ekaterina P / Jobin, Christian / Tumanov, Alexei V

Journal of visualized experiments : JoVE

2016 , Issue 111

Abstract: Intestinal ischemia is a life-threatening condition associated with a broad range of clinical conditions including atherosclerosis, thrombosis, hypotension, necrotizing enterocolitis, bowel transplantation, trauma and chronic inflammation. Intestinal ... ...

Abstract	Intestinal ischemia is a life-threatening condition associated with a broad range of clinical conditions including atherosclerosis, thrombosis, hypotension, necrotizing enterocolitis, bowel transplantation, trauma and chronic inflammation. Intestinal ischemia-reperfusion (IR) injury is a consequence of acute mesenteric ischemia, caused by inadequate blood flow through the mesenteric vessels, resulting in intestinal damage. Reperfusion following ischemia can further exacerbate damage of the intestine. The mechanisms of IR injury are complex and poorly understood. Therefore, experimental small animal models are critical for understanding the pathophysiology of IR injury and the development of novel therapies. Here we describe a mouse model of acute intestinal IR injury that provides reproducible injury of the small intestine without mortality. This is achieved by inducing ischemia in the region of the distal ileum by temporally occluding the peripheral and terminal collateral branches of the superior mesenteric artery for 60 min using microvascular clips. Reperfusion for 1 hr, or 2 hr after injury results in reproducible injury of the intestine examined by histological analysis. Proper position of the microvascular clips is critical for the procedure. Therefore the video clip provides a detailed visual step-by-step description of this technique. This model of intestinal IR injury can be utilized to study the cellular and molecular mechanisms of injury and regeneration.
MeSH term(s)	Animals ; Disease Models, Animal ; Ileum ; Intestine, Small ; Mesenteric Artery, Superior ; Mice ; Reperfusion Injury
Keywords	covid19
Language	English
Publishing date	2016-05-11
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ISSN	1940-087X
ISSN (online)	1940-087X
DOI	10.3791/53881
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Article ; Online: Cytokines, reverse genetics and anti-cytokine therapy

M. S. Drutskaya / E. O. Gubernatorova / E. A. Gorshkova / K.-S. N. Athertkhany / M. A. Nosenko / V. S. Gogoleva / O. A. Namakanova / R. V. Zvartsev / A. A. Kruglov / S. A. Nedospasov

Бюллетень сибирской медицины, Vol 18, Iss 1, Pp 38-

2019 Volume 48

Abstract: Cytokines comprise the molecular language of communication between the cells, which is needed to maintain the homeostatic functions of the body (including the immune system) and mediate various diseases. Many aspects of inflammation, autoimmune diseases ... ...

Abstract	Cytokines comprise the molecular language of communication between the cells, which is needed to maintain the homeostatic functions of the body (including the immune system) and mediate various diseases. Many aspects of inflammation, autoimmune diseases and neoplasia are associated with cytokine signaling through specific receptors. The establishment of new physiological functions of “old” cytokines and understanding the molecular and cellular mechanisms of their involvement in disease pathogenesis, as well as the search for new therapeutic targets and development of innovative approaches to anti-cytokine therapy, present a fundamental problem. When assessing the tremendous success of anti-cytokine therapy in treatment of certain autoimmune diseases, we should not forget that (a) this treatment does not eliminate the causes of the disease:autoreactive T-cell clones; and that (b) less than half of the patients respond to this therapy; and that (c) anti-cytokine therapy has serious side effects.
Keywords	tnf ; il-6 ; мышиные модели ; биспецифические антитела ; коллаген-индуцированный артрит ; экспериментальный аутоиммунный энцефаломиелит ; астма ; гуманизированные мыши ; Medicine ; R
Subject code	610
Language	English
Publishing date	2019-05-01T00:00:00Z
Publisher	Siberian State Medical University (Tomsk)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Macrophages acquire a TNF-dependent inflammatory memory in allergic asthma

2022

Abstract: 2078 ... 2090 ... Background: Infectious agents can reprogram or “train” macrophages and their progenitors to respond more readily to subsequent insults. However, whether such an inflammatory memory exists in type 2 inflammatory conditions such as allergic ... ...

Abstract	2078 2090 Background: Infectious agents can reprogram or “train” macrophages and their progenitors to respond more readily to subsequent insults. However, whether such an inflammatory memory exists in type 2 inflammatory conditions such as allergic asthma was not known. Objective: We sought to decipher macrophage-trained immunity in allergic asthma. Methods: We used a combination of clinical sampling of house dust mite (HDM)-allergic patients, HDM-induced allergic airway inflammation in mice, and an in vitro training setup to analyze persistent changes in macrophage eicosanoid, cytokine, and chemokine production as well as the underlying metabolic and epigenetic mechanisms. Transcriptional and metabolic profiles of patient-derived and in vitro trained macrophages were assessed by RNA sequencing or metabolic flux analysis and liquid chromatography-tandem mass spectrometry analysis, respectively. Results: We found that macrophages differentiated from bone marrow or blood monocyte progenitors of HDM-allergic mice or asthma patients show inflammatory transcriptional reprogramming and excessive mediator (TNF-α, CCL17, leukotriene, PGE2, IL-6) responses upon stimulation. Macrophages from HDM-allergic mice initially exhibited a type 2 imprint, which shifted toward a classical inflammatory training over time. HDM-induced allergic airway inflammation elicited a metabolically activated macrophage phenotype, producing high amounts of 2-hydroxyglutarate (2-HG). HDM-induced macrophage training in vitro was mediated by a formyl peptide receptor 2–TNF-2-HG-PGE2/PGE2 receptor 2 axis, resulting in an M2-like macrophage phenotype with high CCL17 production. TNF blockade by etanercept or genetic ablation of Tnf in myeloid cells prevented the inflammatory imprinting of bone marrow-derived macrophages from HDM-allergic mice. Conclusion: Allergen-triggered inflammation drives a TNF-dependent innate memory, which may perpetuate and exacerbate chronic type 2 airway inflammation and thus represents a target for asthma therapy. 149 ...
Keywords	CCL17 ; chemokines ; eicosanoids ; lipid mediators ; macrophages ; trained immunity ; type 2 inflammation
Subject code	610
Language	English
Publishing country	de
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Macrophages acquire a TNF-dependent inflammatory memory in allergic asthma.

The Journal of allergy and clinical immunology

2021 Volume 149, Issue 6, Page(s) 2078–2090

Abstract: Background: Infectious agents can reprogram or "train" macrophages and their progenitors to respond more readily to subsequent insults. However, whether such an inflammatory memory exists in type 2 inflammatory conditions such as allergic asthma was not ...

Abstract	Background: Infectious agents can reprogram or "train" macrophages and their progenitors to respond more readily to subsequent insults. However, whether such an inflammatory memory exists in type 2 inflammatory conditions such as allergic asthma was not known. Objective: We sought to decipher macrophage-trained immunity in allergic asthma. Methods: We used a combination of clinical sampling of house dust mite (HDM)-allergic patients, HDM-induced allergic airway inflammation in mice, and an in vitro training setup to analyze persistent changes in macrophage eicosanoid, cytokine, and chemokine production as well as the underlying metabolic and epigenetic mechanisms. Transcriptional and metabolic profiles of patient-derived and in vitro trained macrophages were assessed by RNA sequencing or metabolic flux analysis and liquid chromatography-tandem mass spectrometry analysis, respectively. Results: We found that macrophages differentiated from bone marrow or blood monocyte progenitors of HDM-allergic mice or asthma patients show inflammatory transcriptional reprogramming and excessive mediator (TNF-α, CCL17, leukotriene, PGE Conclusion: Allergen-triggered inflammation drives a TNF-dependent innate memory, which may perpetuate and exacerbate chronic type 2 airway inflammation and thus represents a target for asthma therapy.
MeSH term(s)	Animals ; Asthma ; Dermatophagoides pteronyssinus ; Disease Models, Animal ; Humans ; Hypersensitivity ; Inflammation ; Macrophages ; Mice ; Prostaglandins E/metabolism ; Pyroglyphidae
Chemical Substances	Prostaglandins E
Language	English
Publishing date	2021-12-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2021.11.026
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