Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats
Our objective was to develop a model of systemic inflammatory response syndrome (SIRS) by chemical induction of colon injury and antibiotic-associated intestinal dysbiosis in rats with primary visceral obesity (PVO) for studies of myocardial resistance to ischemia-reperfusion injury. The experiments...
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St. Petersburg branch of the Russian Association of Allergologists and Clinical Immunologists
2020-01-01
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Series: | Медицинская иммунология |
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Online Access: | https://www.mimmun.ru/mimmun/article/view/1839 |
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author | Yu. Yu. Borschev I. Yu. Burovenko A. B. Karaseva S. M. Minasyan V. Yu. Borschev N. Yu. Semenova O. V. Borshcheva V. V. Polovinkin G. G. Rodionov A. N. Suvorov M. M. Galagudza |
author_facet | Yu. Yu. Borschev I. Yu. Burovenko A. B. Karaseva S. M. Minasyan V. Yu. Borschev N. Yu. Semenova O. V. Borshcheva V. V. Polovinkin G. G. Rodionov A. N. Suvorov M. M. Galagudza |
author_sort | Yu. Yu. Borschev |
collection | DOAJ |
description | Our objective was to develop a model of systemic inflammatory response syndrome (SIRS) by chemical induction of colon injury and antibiotic-associated intestinal dysbiosis in rats with primary visceral obesity (PVO) for studies of myocardial resistance to ischemia-reperfusion injury. The experiments were performed with adult Wistar male rats with PVO under improved conditions of a conventional animal clinic. The chemically induced inflammatory colon disease (CIICD) was accomplished by intragastric administration of a mixture of broad-spectrum antimicrobial agents (AMA) for 3 days. Five days later, immunological and biochemical studies were carried out, as follows: composition of the intestinal microbiota in feces and shortchain fatty acids in blood, morphological changes in the structure of the colon, hemodynamic parameters and myocardial stability with modified Langendorff system. In PVO rats, the mass of visceral fat deposits and the content of lipopolysaccharides (LPS) in the blood were significantly increased when giving them fatcarbohydrate diet (FCD). In animals with CIICD, in addition to LPS, there was a significant increase in proinflammatory cytokine concentration (TNF, IL-8, MCP-1), and after oral administration of the AMA mixture, pronounced disturbances of food behavior and evacuatory function of gastrointestinal tract, deep destructive changes in colon, as well as qualitative and quantitative composition of intestinal microbiota with characteristics typical to the first-grade dysbiosis. High levels were shown for IL-8 cytokine only. An increase in acetic and propionic acid concentrations were shown in blood in animals with CIICD, and, to a greater extent, in rats with antibiotic-induced dysbiosis (AID). FCD was followed by significantly reduced levels of lactobacilli and bifidobacteria in colonic contents. CIICD leads to detection of Escherichia coli, and intestinal dysbiosis leads to the manifestation of Proteus. A comorbid combination of pathological changes in the immune and digestive systems caused a significant increase in the area of myocardial necrosis (by 35 percent) in isolated heart by, thus presuming decreased myocardial resistance to ischemia-reperfusion injury (IRI). The SIRS model induced by chemical trauma to large intestine is aggravated by the introduction of AMAs mixture, and it is characterized by a controlled change in inflammatory markers. Deterioration of morphofunctional characteristics in isolated heart included decrease in resistance to IRI seems to correspond to acute inflammatory bowel disease with induced intestinal dysbiosis. This model can be used in experimental medicine in the field of cardiology, endomicroecology, gastroenterology, and immunology. |
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series | Медицинская иммунология |
spelling | doaj.art-b7f93259c7ce4f4698434544cdc320122024-04-22T13:07:44ZrusSt. Petersburg branch of the Russian Association of Allergologists and Clinical ImmunologistsМедицинская иммунология1563-06252313-741X2020-01-01221879810.15789/1563-0625-MOS-18391211Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in ratsYu. Yu. Borschev0I. Yu. Burovenko1A. B. Karaseva2S. M. Minasyan3V. Yu. Borschev4N. Yu. Semenova5O. V. Borshcheva6V. V. Polovinkin7G. G. Rodionov8A. N. Suvorov9M. M. Galagudza10V. Almazov National Medical Research Centre; LLC “Research Center Probiocode SP”V. Almazov National Medical Research Centre; T. Shevchenko Pridnestrovian State UniversityInstitute of Experimental MedicineV. Almazov National Medical Research Centre; First St. Petersburg State I. Pavlov Medical UniversityTechnical University of MoldovaV. Almazov National Medical Research CentreV. Almazov National Medical Research CentreResearch Institute – S. Ochapovsky Regional Clinical Hospital No. 1А. Nikiforov Russian Center of Emergency and Radiation MedicineInstitute of Experimental Medicine; St. Petersburg State UniversityV. Almazov National Medical Research Centre; First St. Petersburg State I. Pavlov Medical UniversityOur objective was to develop a model of systemic inflammatory response syndrome (SIRS) by chemical induction of colon injury and antibiotic-associated intestinal dysbiosis in rats with primary visceral obesity (PVO) for studies of myocardial resistance to ischemia-reperfusion injury. The experiments were performed with adult Wistar male rats with PVO under improved conditions of a conventional animal clinic. The chemically induced inflammatory colon disease (CIICD) was accomplished by intragastric administration of a mixture of broad-spectrum antimicrobial agents (AMA) for 3 days. Five days later, immunological and biochemical studies were carried out, as follows: composition of the intestinal microbiota in feces and shortchain fatty acids in blood, morphological changes in the structure of the colon, hemodynamic parameters and myocardial stability with modified Langendorff system. In PVO rats, the mass of visceral fat deposits and the content of lipopolysaccharides (LPS) in the blood were significantly increased when giving them fatcarbohydrate diet (FCD). In animals with CIICD, in addition to LPS, there was a significant increase in proinflammatory cytokine concentration (TNF, IL-8, MCP-1), and after oral administration of the AMA mixture, pronounced disturbances of food behavior and evacuatory function of gastrointestinal tract, deep destructive changes in colon, as well as qualitative and quantitative composition of intestinal microbiota with characteristics typical to the first-grade dysbiosis. High levels were shown for IL-8 cytokine only. An increase in acetic and propionic acid concentrations were shown in blood in animals with CIICD, and, to a greater extent, in rats with antibiotic-induced dysbiosis (AID). FCD was followed by significantly reduced levels of lactobacilli and bifidobacteria in colonic contents. CIICD leads to detection of Escherichia coli, and intestinal dysbiosis leads to the manifestation of Proteus. A comorbid combination of pathological changes in the immune and digestive systems caused a significant increase in the area of myocardial necrosis (by 35 percent) in isolated heart by, thus presuming decreased myocardial resistance to ischemia-reperfusion injury (IRI). The SIRS model induced by chemical trauma to large intestine is aggravated by the introduction of AMAs mixture, and it is characterized by a controlled change in inflammatory markers. Deterioration of morphofunctional characteristics in isolated heart included decrease in resistance to IRI seems to correspond to acute inflammatory bowel disease with induced intestinal dysbiosis. This model can be used in experimental medicine in the field of cardiology, endomicroecology, gastroenterology, and immunology.https://www.mimmun.ru/mimmun/article/view/1839cytokinesinflammatory colon diseaseantibiotic-induced dysbiosisisolated heartinfarct size |
spellingShingle | Yu. Yu. Borschev I. Yu. Burovenko A. B. Karaseva S. M. Minasyan V. Yu. Borschev N. Yu. Semenova O. V. Borshcheva V. V. Polovinkin G. G. Rodionov A. N. Suvorov M. M. Galagudza Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats Медицинская иммунология cytokines inflammatory colon disease antibiotic-induced dysbiosis isolated heart infarct size |
title | Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats |
title_full | Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats |
title_fullStr | Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats |
title_full_unstemmed | Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats |
title_short | Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats |
title_sort | modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats |
topic | cytokines inflammatory colon disease antibiotic-induced dysbiosis isolated heart infarct size |
url | https://www.mimmun.ru/mimmun/article/view/1839 |
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