Pathogenesis of the inflammatory bowel disease in context of SARS-COV-2 infection

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Pathogenesis of the inflammatory bowel disease in context of SARS-COV-2 infection. / Dvornikova, K. A.; Bystrova, E. Yu; Churilov, L. P.; Lerner, A.

In: Molecular Biology Reports, Vol. 48, No. 7, 07.2021, p. 5745-5758.

Research output: Contribution to journal › Review article › peer-review

BibTeX

@article{8f0e71c806e446cf8e151eff7aa3f3b6,

title = "Pathogenesis of the inflammatory bowel disease in context of SARS-COV-2 infection",

abstract = "To date, the latest research results suggest that the novel severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) can enter host cells directly via the gastrointestinal tract by binding to the enterocyte-expressed ACE2 receptor, or indirectly as a result of infection of type II alveolar epithelial cells. At the same time, entry of SARS-CoV-2 through the gastrointestinal tract initiates the activation of innate and adaptive immune responses, the formation of an excessive inflammatory reaction and critical increase in the expression of proinflammatory cytokines, which, subsequently, can presumably increase inflammation and induce intestinal damage in patients suffering from inflammatory bowel disease (IBD). The aims of the present review were to reveal and analyze possible molecular pathways and consequences of the induction of an innate and adaptive immune response during infection with SARS-CoV-2 in patients with IBD. A thorough literature search was carried out by using the keywords: IBD, SARS-CoV-2, COVID-19. Based on the screening, a number of intracellular and extracellular pathways were considered and discussed, which can impact the immune response during SARS-CoV-2 infection in IBD patients. Additionally, the possible consequences of the infection for such patients were estimated. We further hypothesize that any virus, including the new SARS-CoV-2, infecting intestinal tissues and/or entering the host{\textquoteright}s body through receptors located on intestinal enterocytes may be a trigger for the onset of IBD in individuals with a genetic predisposition and/or the risk of developing IBD associated with other factors.",

keywords = "Adaptive immunity, COVID-19, Crohn{\textquoteright}s disease, Inflammatory bowel disease, Innate immunity, SARS-CoV-2, Toll-like receptors, Ulcerative colitis, Adaptive Immunity, Humans, Receptors, Virus/immunology, Immunity, Innate, Virus Internalization, Inflammatory Bowel Diseases/epidemiology, COVID-19/epidemiology, SARS-CoV-2/immunology, Gastrointestinal Tract/immunology",

author = "Dvornikova, {K. A.} and Bystrova, {E. Yu} and Churilov, {L. P.} and A. Lerner",

note = "Publisher Copyright: {\textcopyright} 2021, The Author(s), under exclusive licence to Springer Nature B.V.",

year = "2021",

month = jul,

doi = "10.1007/s11033-021-06565-w",

language = "English",

volume = "48",

pages = "5745--5758",

journal = "Molecular Biology Reports",

issn = "0301-4851",

publisher = "Springer Nature",

number = "7",

}

RIS

TY - JOUR

T1 - Pathogenesis of the inflammatory bowel disease in context of SARS-COV-2 infection

AU - Dvornikova, K. A.

AU - Bystrova, E. Yu

AU - Churilov, L. P.

AU - Lerner, A.

PY - 2021/7

Y1 - 2021/7

N2 - To date, the latest research results suggest that the novel severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) can enter host cells directly via the gastrointestinal tract by binding to the enterocyte-expressed ACE2 receptor, or indirectly as a result of infection of type II alveolar epithelial cells. At the same time, entry of SARS-CoV-2 through the gastrointestinal tract initiates the activation of innate and adaptive immune responses, the formation of an excessive inflammatory reaction and critical increase in the expression of proinflammatory cytokines, which, subsequently, can presumably increase inflammation and induce intestinal damage in patients suffering from inflammatory bowel disease (IBD). The aims of the present review were to reveal and analyze possible molecular pathways and consequences of the induction of an innate and adaptive immune response during infection with SARS-CoV-2 in patients with IBD. A thorough literature search was carried out by using the keywords: IBD, SARS-CoV-2, COVID-19. Based on the screening, a number of intracellular and extracellular pathways were considered and discussed, which can impact the immune response during SARS-CoV-2 infection in IBD patients. Additionally, the possible consequences of the infection for such patients were estimated. We further hypothesize that any virus, including the new SARS-CoV-2, infecting intestinal tissues and/or entering the host’s body through receptors located on intestinal enterocytes may be a trigger for the onset of IBD in individuals with a genetic predisposition and/or the risk of developing IBD associated with other factors.

AB - To date, the latest research results suggest that the novel severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) can enter host cells directly via the gastrointestinal tract by binding to the enterocyte-expressed ACE2 receptor, or indirectly as a result of infection of type II alveolar epithelial cells. At the same time, entry of SARS-CoV-2 through the gastrointestinal tract initiates the activation of innate and adaptive immune responses, the formation of an excessive inflammatory reaction and critical increase in the expression of proinflammatory cytokines, which, subsequently, can presumably increase inflammation and induce intestinal damage in patients suffering from inflammatory bowel disease (IBD). The aims of the present review were to reveal and analyze possible molecular pathways and consequences of the induction of an innate and adaptive immune response during infection with SARS-CoV-2 in patients with IBD. A thorough literature search was carried out by using the keywords: IBD, SARS-CoV-2, COVID-19. Based on the screening, a number of intracellular and extracellular pathways were considered and discussed, which can impact the immune response during SARS-CoV-2 infection in IBD patients. Additionally, the possible consequences of the infection for such patients were estimated. We further hypothesize that any virus, including the new SARS-CoV-2, infecting intestinal tissues and/or entering the host’s body through receptors located on intestinal enterocytes may be a trigger for the onset of IBD in individuals with a genetic predisposition and/or the risk of developing IBD associated with other factors.

KW - Adaptive immunity

KW - COVID-19

KW - Crohn’s disease

KW - Inflammatory bowel disease

KW - Innate immunity

KW - SARS-CoV-2

KW - Toll-like receptors

KW - Ulcerative colitis

KW - Adaptive Immunity

KW - Humans

KW - Receptors, Virus/immunology

KW - Immunity, Innate

KW - Virus Internalization

KW - Inflammatory Bowel Diseases/epidemiology

KW - COVID-19/epidemiology

KW - SARS-CoV-2/immunology

KW - Gastrointestinal Tract/immunology

UR - http://www.scopus.com/inward/record.url?scp=85111088657&partnerID=8YFLogxK

UR - https://www.mendeley.com/catalogue/5bafaca4-9cca-3140-84f9-5a598d76930b/

U2 - 10.1007/s11033-021-06565-w

DO - 10.1007/s11033-021-06565-w

M3 - Review article

C2 - 34296352

AN - SCOPUS:85111088657

VL - 48

SP - 5745

EP - 5758

JO - Molecular Biology Reports

JF - Molecular Biology Reports

SN - 0301-4851

IS - 7

ER -

ID: 84644364