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Trichinella spiralis Infection Suppressed Gut Inflammation with CD4(+)CD25(+)Foxp3(+) T Cell Recruitment

In order to know the effect of pre-existing Trichinella spiralis infection on experimentally induced intestinal inflammation and immune responses, we induced colitis in T. spiralis-infected mice and observed the severity of colitis and the levels of Th1, Th2, and regulatory cytokines and recruitment...

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Detalles Bibliográficos
Autores principales: Cho, Min Kyoung, Park, Mi Kyung, Kang, Shin Ae, Choi, Seon Hee, Ahn, Soon Cheol, Yu, Hak Sun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society for Parasitology and Tropical Medicine 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514436/
https://www.ncbi.nlm.nih.gov/pubmed/23230342
http://dx.doi.org/10.3347/kjp.2012.50.4.385
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author Cho, Min Kyoung
Park, Mi Kyung
Kang, Shin Ae
Choi, Seon Hee
Ahn, Soon Cheol
Yu, Hak Sun
author_facet Cho, Min Kyoung
Park, Mi Kyung
Kang, Shin Ae
Choi, Seon Hee
Ahn, Soon Cheol
Yu, Hak Sun
author_sort Cho, Min Kyoung
collection PubMed
description In order to know the effect of pre-existing Trichinella spiralis infection on experimentally induced intestinal inflammation and immune responses, we induced colitis in T. spiralis-infected mice and observed the severity of colitis and the levels of Th1, Th2, and regulatory cytokines and recruitment of CD4(+)CD25(+)Foxp3(+) T (regulatory T; T(reg)) cells. Female C57BL/6 mice were infected with 250 muscle larvae; after 4 weeks, induction of experimental colitis was performed using 3% dextran sulfate sodium (DSS). During the induction period, we observed severity of colitis, including weight loss and status of stool, and evaluated the disease activity index (DAI). A significantly low DAI and degree of weight loss were observed in infected mice, compared with uninfected mice. In addition, colon length in infected mice was not contracted, compared with uninfected mice. We also observed a significant increase in production of pro-inflammatory cytokines, IL-6 and IFN-γ, in spleen lymphocytes treated with DSS; however, such an increase was not observed in infected mice treated with DSS. Of particular interest, production of regulatory cytokines, IL-10 and transforming growth factor (TGF)-β, in spleen lymphocytes showed a significant increase in mice infected with T. spiralis. A similar result was observed in mesenteric lymph nodes (MLN). Subsets of the population of T(reg) cells in MLN and spleen showed significant increases in mice infected with T. spiralis. In conclusion, T. spiralis infection can inhibit the DSS-induced colitis in mice by enhancing the regulatory cytokine and T(reg) cells recruitment.
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spelling pubmed-35144362012-12-10 Trichinella spiralis Infection Suppressed Gut Inflammation with CD4(+)CD25(+)Foxp3(+) T Cell Recruitment Cho, Min Kyoung Park, Mi Kyung Kang, Shin Ae Choi, Seon Hee Ahn, Soon Cheol Yu, Hak Sun Korean J Parasitol Brief Communication In order to know the effect of pre-existing Trichinella spiralis infection on experimentally induced intestinal inflammation and immune responses, we induced colitis in T. spiralis-infected mice and observed the severity of colitis and the levels of Th1, Th2, and regulatory cytokines and recruitment of CD4(+)CD25(+)Foxp3(+) T (regulatory T; T(reg)) cells. Female C57BL/6 mice were infected with 250 muscle larvae; after 4 weeks, induction of experimental colitis was performed using 3% dextran sulfate sodium (DSS). During the induction period, we observed severity of colitis, including weight loss and status of stool, and evaluated the disease activity index (DAI). A significantly low DAI and degree of weight loss were observed in infected mice, compared with uninfected mice. In addition, colon length in infected mice was not contracted, compared with uninfected mice. We also observed a significant increase in production of pro-inflammatory cytokines, IL-6 and IFN-γ, in spleen lymphocytes treated with DSS; however, such an increase was not observed in infected mice treated with DSS. Of particular interest, production of regulatory cytokines, IL-10 and transforming growth factor (TGF)-β, in spleen lymphocytes showed a significant increase in mice infected with T. spiralis. A similar result was observed in mesenteric lymph nodes (MLN). Subsets of the population of T(reg) cells in MLN and spleen showed significant increases in mice infected with T. spiralis. In conclusion, T. spiralis infection can inhibit the DSS-induced colitis in mice by enhancing the regulatory cytokine and T(reg) cells recruitment. The Korean Society for Parasitology and Tropical Medicine 2012-12 2012-11-26 /pmc/articles/PMC3514436/ /pubmed/23230342 http://dx.doi.org/10.3347/kjp.2012.50.4.385 Text en © 2012, Korean Society for Parasitology and Tropical Medicine http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Brief Communication
Cho, Min Kyoung
Park, Mi Kyung
Kang, Shin Ae
Choi, Seon Hee
Ahn, Soon Cheol
Yu, Hak Sun
Trichinella spiralis Infection Suppressed Gut Inflammation with CD4(+)CD25(+)Foxp3(+) T Cell Recruitment
title Trichinella spiralis Infection Suppressed Gut Inflammation with CD4(+)CD25(+)Foxp3(+) T Cell Recruitment
title_full Trichinella spiralis Infection Suppressed Gut Inflammation with CD4(+)CD25(+)Foxp3(+) T Cell Recruitment
title_fullStr Trichinella spiralis Infection Suppressed Gut Inflammation with CD4(+)CD25(+)Foxp3(+) T Cell Recruitment
title_full_unstemmed Trichinella spiralis Infection Suppressed Gut Inflammation with CD4(+)CD25(+)Foxp3(+) T Cell Recruitment
title_short Trichinella spiralis Infection Suppressed Gut Inflammation with CD4(+)CD25(+)Foxp3(+) T Cell Recruitment
title_sort trichinella spiralis infection suppressed gut inflammation with cd4(+)cd25(+)foxp3(+) t cell recruitment
topic Brief Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514436/
https://www.ncbi.nlm.nih.gov/pubmed/23230342
http://dx.doi.org/10.3347/kjp.2012.50.4.385
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