Print Email Facebook Twitter Gene expression profiling identifies mechanisms of protection to recurrent trinitrobenzene sulfonic acid colitis mediated by probiotics Title Gene expression profiling identifies mechanisms of protection to recurrent trinitrobenzene sulfonic acid colitis mediated by probiotics Author Mariman, R. Kremer, S.H.A. van Erk, M. Lagerweij, T. Koning, F. Nagelkerken, L. Publication year 2012 Abstract Background: Host-microbiota interactions in the intestinal mucosa play a major role in intestinal immune homeostasis and control the threshold of local inflammation. The aim of this study was to evaluate the efficacy of probiotics in the recurrent trinitrobenzene sulfonic acid (TNBS)-induced colitis model and gain more insight into protective mechanisms. Methods: Moderate chronic inflammation of the colon was induced in BALB/c mice by repetitive intrarectal challenges with TNBS. Administration of probiotics started 2 weeks before colitis induction and was continued throughout colitis development. Results: Long-term administration of Lactobacillus plantarum NCIMB8826 or the probiotic mixture VSL#3 reduced intestinal inflammation induced by TNBS, evident from improved colon morphology and less influx of innate (CD11b+) and adaptive (CD4+/CD8+) immune cells in the intestinal mucosa and decreased proinflammatory serum cytokines (interferon-gamma [IFN-γ], interleukin [IL]-17, IL-1β, monocyte chemoattractant protein [MCP]-1) in probiotic-treated mice. Genomewide expression analysis of colonic tissues using microarrays revealed differences in expression of genes related to inflammation and immune processes between untreated and probiotic treated mice. Principal component analysis revealed that probiotic treatment resulted in a shift of gene expression profiles toward those of healthy controls. Effects of probiotics on colonic gene expression were most profound during active inflammation, in particular on gene clusters related to mast cells and antimicrobial peptides. The results were substantiated by suppression of chemokine gene expression. Conclusions: Our data are in favor of a model in which probiotics downregulate expression of chemokines in the colon, thereby decreasing influx of inflammatory cells and rendering mice resistant to the induction of colitis. Copyright © 2011 Crohn's & Colitis Foundation of America, Inc. Chemicals/CAS: alpha defensin, 251460-81-8; carboxypeptidase A, 11075-17-5; chymase, 75496-62-7, 97501-92-3; gamma interferon, 82115-62-6; macrophage inflammatory protein 1alpha, 155075-84-6; trinitrobenzenesulfonic acid, 16655-63-3, 2508-19-2 Subject LifeMHR - Metabolic Health Research MSB - Microbiology and Systems BiologyEELS - Earth, Environmental and Life SciencesBiomedical InnovationBiologyHealthy Livinggenome wide screeningimmune modulationprobiotic bacteriaTNBS colitisalpha defensincarboxypeptidase ACD11b antigenchymasegamma interferongranulocyte colony stimulating factorgranulocyte macrophage colony stimulating factorinterleukin 10interleukin 17interleukin 1alphainterleukin 1betainterleukin 3interleukin 9macrophage inflammatory protein 1alphamonocyte chemotactic protein 1polypeptide antibiotic agentprobiotic agenttrinitrobenzenesulfonic acidabscessadaptive immunityanimal experimentanimal modelanimal tissuearticleCD4 CD8 ratioCD4+ T lymphocyteCD8+ T lymphocytecell activitycell infiltrationchronic inflammationcolitiscolon mucosacontrolled studydrug efficacyenteritisfemalegene expressiongoblet cellhistopathologyimmunocompetent cellinflammatory cellintestine mucosaLactobacillus plantarumlong term caremast cellmicroarray analysismousenonhumanpriority journalupregulationweight reduction To reference this document use: http://resolver.tudelft.nl/uuid:5b1c59ef-5bd2-4974-8845-6e3699bc5c0e DOI https://doi.org/10.1002/ibd.22849 TNO identifier 462866 ISSN 1078-0998 Source Inflammatory Bowel Diseases, 18 (8), 1424-1433 Document type article Files To receive the publication files, please send an e-mail request to TNO Library.