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EXPRESSION OF E-CADHERIN AND CLAUDIN-3 IN THE COLONIC EPITHELIUM AFTER THE INFLIXIMAB THERAPY: EXPERIMENTAL MODEL OF DISUSE COLITIS

The etiopathogenesis of disuse colitis (DC) has not yet been fully elucidated. The main theories consider that the disease may be related to an increase in anaerobic bacteria, the lack of short-chain fatty acid (SCFA) supply, and immunological disorders that develop in the colorectal segments devoid...

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Autores principales: ALVES, Antonio José Tiburcio, GOTO, Eduardo Felipe Kim, PEREIRA, José Aires, DOMINGUES, Fernanda Aparecida, de ÁVILA, Mariane Grandi, COY, Claudio Saddy Rodrigues, MARTINEZ, Carlos Augusto Real
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Colégio Brasileiro de Cirurgia Digestiva 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8846491/
https://www.ncbi.nlm.nih.gov/pubmed/35107501
http://dx.doi.org/10.1590/0102-672020210002e1639
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author ALVES, Antonio José Tiburcio
GOTO, Eduardo Felipe Kim
PEREIRA, José Aires
DOMINGUES, Fernanda Aparecida
de ÁVILA, Mariane Grandi
COY, Claudio Saddy Rodrigues
MARTINEZ, Carlos Augusto Real
author_facet ALVES, Antonio José Tiburcio
GOTO, Eduardo Felipe Kim
PEREIRA, José Aires
DOMINGUES, Fernanda Aparecida
de ÁVILA, Mariane Grandi
COY, Claudio Saddy Rodrigues
MARTINEZ, Carlos Augusto Real
author_sort ALVES, Antonio José Tiburcio
collection PubMed
description The etiopathogenesis of disuse colitis (DC) has not yet been fully elucidated. The main theories consider that the disease may be related to an increase in anaerobic bacteria, the lack of short-chain fatty acid (SCFA) supply, and immunological disorders that develop in the colorectal segments devoid of fecal transit. AIM: The aim of this study was to verify whether the application of infliximab modifies the tissue content of E-cadherin and claudin-3 proteins in colonic epithelium of rats devoid of intestinal transit. METHODS: A total of 22 rats underwent intestinal transit bypass using Hartmann’s procedure. They remained with the shunt for 12 weeks to allow the development of DC. Later, they were divided into three experimental groups: six animals received 2.0 mL saline solution/week, eight received infliximab at a dose of 5 mg/kg/week, and eight received infliximab at a dose of 10 mg/kg/week for 5 consecutive weeks. At the end of this period, the animals were euthanized, and the colonic segments with and without intestinal transit were removed. DC was diagnosed based on the histological changes defined by a previously validated scale. The tissue expression of E-cadherin and claudin-3 was assessed by immunohistochemistry, and the tissue content of both proteins was quantified by computer-aided image analysis. RESULTS: The colonic segments excluded from fecal transit showed a higher degree of inflammation than those exposed to fecal transit. The degree of inflammation was lower in animals treated with infliximab, regardless of the dose used. The levels of E-cadherin and claudin-3 were reduced in the excluded colon. Treating animals with infliximab increased the levels of both proteins in the colonic segments without intestinal transit, especially in animals receiving a dose of 10 mg/kg/week. CONCLUSION: Infliximab therapy reduces inflammation in the colonic segments excluded from intestinal transit and increases the tissue content of E-cadherin and claudin-3 proteins, especially when used at a concentration of 10 mg/kg/week.
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spelling pubmed-88464912022-02-28 EXPRESSION OF E-CADHERIN AND CLAUDIN-3 IN THE COLONIC EPITHELIUM AFTER THE INFLIXIMAB THERAPY: EXPERIMENTAL MODEL OF DISUSE COLITIS ALVES, Antonio José Tiburcio GOTO, Eduardo Felipe Kim PEREIRA, José Aires DOMINGUES, Fernanda Aparecida de ÁVILA, Mariane Grandi COY, Claudio Saddy Rodrigues MARTINEZ, Carlos Augusto Real Arq Bras Cir Dig Artigo Original The etiopathogenesis of disuse colitis (DC) has not yet been fully elucidated. The main theories consider that the disease may be related to an increase in anaerobic bacteria, the lack of short-chain fatty acid (SCFA) supply, and immunological disorders that develop in the colorectal segments devoid of fecal transit. AIM: The aim of this study was to verify whether the application of infliximab modifies the tissue content of E-cadherin and claudin-3 proteins in colonic epithelium of rats devoid of intestinal transit. METHODS: A total of 22 rats underwent intestinal transit bypass using Hartmann’s procedure. They remained with the shunt for 12 weeks to allow the development of DC. Later, they were divided into three experimental groups: six animals received 2.0 mL saline solution/week, eight received infliximab at a dose of 5 mg/kg/week, and eight received infliximab at a dose of 10 mg/kg/week for 5 consecutive weeks. At the end of this period, the animals were euthanized, and the colonic segments with and without intestinal transit were removed. DC was diagnosed based on the histological changes defined by a previously validated scale. The tissue expression of E-cadherin and claudin-3 was assessed by immunohistochemistry, and the tissue content of both proteins was quantified by computer-aided image analysis. RESULTS: The colonic segments excluded from fecal transit showed a higher degree of inflammation than those exposed to fecal transit. The degree of inflammation was lower in animals treated with infliximab, regardless of the dose used. The levels of E-cadherin and claudin-3 were reduced in the excluded colon. Treating animals with infliximab increased the levels of both proteins in the colonic segments without intestinal transit, especially in animals receiving a dose of 10 mg/kg/week. CONCLUSION: Infliximab therapy reduces inflammation in the colonic segments excluded from intestinal transit and increases the tissue content of E-cadherin and claudin-3 proteins, especially when used at a concentration of 10 mg/kg/week. Colégio Brasileiro de Cirurgia Digestiva 2022-01-31 /pmc/articles/PMC8846491/ /pubmed/35107501 http://dx.doi.org/10.1590/0102-672020210002e1639 Text en https://creativecommons.org/licenses/by/4.0/Este é um artigo publicado em acesso aberto sob uma licença Creative Commons
spellingShingle Artigo Original
ALVES, Antonio José Tiburcio
GOTO, Eduardo Felipe Kim
PEREIRA, José Aires
DOMINGUES, Fernanda Aparecida
de ÁVILA, Mariane Grandi
COY, Claudio Saddy Rodrigues
MARTINEZ, Carlos Augusto Real
EXPRESSION OF E-CADHERIN AND CLAUDIN-3 IN THE COLONIC EPITHELIUM AFTER THE INFLIXIMAB THERAPY: EXPERIMENTAL MODEL OF DISUSE COLITIS
title EXPRESSION OF E-CADHERIN AND CLAUDIN-3 IN THE COLONIC EPITHELIUM AFTER THE INFLIXIMAB THERAPY: EXPERIMENTAL MODEL OF DISUSE COLITIS
title_full EXPRESSION OF E-CADHERIN AND CLAUDIN-3 IN THE COLONIC EPITHELIUM AFTER THE INFLIXIMAB THERAPY: EXPERIMENTAL MODEL OF DISUSE COLITIS
title_fullStr EXPRESSION OF E-CADHERIN AND CLAUDIN-3 IN THE COLONIC EPITHELIUM AFTER THE INFLIXIMAB THERAPY: EXPERIMENTAL MODEL OF DISUSE COLITIS
title_full_unstemmed EXPRESSION OF E-CADHERIN AND CLAUDIN-3 IN THE COLONIC EPITHELIUM AFTER THE INFLIXIMAB THERAPY: EXPERIMENTAL MODEL OF DISUSE COLITIS
title_short EXPRESSION OF E-CADHERIN AND CLAUDIN-3 IN THE COLONIC EPITHELIUM AFTER THE INFLIXIMAB THERAPY: EXPERIMENTAL MODEL OF DISUSE COLITIS
title_sort expression of e-cadherin and claudin-3 in the colonic epithelium after the infliximab therapy: experimental model of disuse colitis
topic Artigo Original
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8846491/
https://www.ncbi.nlm.nih.gov/pubmed/35107501
http://dx.doi.org/10.1590/0102-672020210002e1639
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