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1.
Mol Biol Rep ; 48(7): 5745-5758, 2021 Jul.
Article in English | MEDLINE | ID: mdl-34296352

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'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.


Subject(s)
Adaptive Immunity , COVID-19/epidemiology , Gastrointestinal Tract , Immunity, Innate , Inflammatory Bowel Diseases , COVID-19/immunology , COVID-19/virology , Gastrointestinal Tract/immunology , Gastrointestinal Tract/pathology , Gastrointestinal Tract/virology , Humans , Inflammatory Bowel Diseases/epidemiology , Inflammatory Bowel Diseases/immunology , Receptors, Virus/immunology , SARS-CoV-2/immunology , SARS-CoV-2/physiology , Virus Internalization
2.
Bull Exp Biol Med ; 159(2): 248-52, 2015 Jun.
Article in English | MEDLINE | ID: mdl-26085359

ABSTRACT

Immunohistochemical assay with double label and confocal laser scanning microscopy showed that innate immunity receptor TLR4 is expressed predominantly in neurons of the intestinal Auerbach (myenteric) plexus, while vanilloid nociceptive receptor TRPV1 is expressed by neurons of Meissner (submucous) plexus. Immunohistochemical analysis with triple labeling revealed coexpression of TLR4 and TRPV1 in enteric neurons of rat colon. The results attest to a possibility of functional interaction between Toll-like and vanilloid receptors in the neuron level.


Subject(s)
Colon/innervation , Myenteric Plexus/metabolism , Nociceptors/metabolism , Receptors, Pattern Recognition/metabolism , Submucous Plexus/metabolism , TRPV Cation Channels/metabolism , Toll-Like Receptor 4/metabolism , Animals , Colon/metabolism , Immunohistochemistry , Male , Microscopy, Confocal , Rats , Rats, Sprague-Dawley , Statistics, Nonparametric
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