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Characterization of FasL expression of rat Mesenteric Lymph Node Dendritic Cells during Inflammatory Bowel Disease (IBD)
Author(s) -
Rivera Edelmarie,
Rodriguez Freddy,
Appleyard Caroline Barbara
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1012.1
Subject(s) - cecum , mesenteric lymph nodes , fas ligand , pathogenesis , medicine , inflammatory bowel disease , immunology , immune system , colitis , flow cytometry , lymph node , lymph , apoptosis , pathology , biology , disease , programmed cell death , biochemistry
Strong evidence demonstrates that a breakdown of tolerance against intestinal microflora is a major factor in the pathogenesis of IBD. Dendritic cells (DCs) appear to play a role in modulating the innate and adaptive immune response. During IBD DCs are activated and the toll like receptors upregulated. The DC populations present in inflamed and control mesenteric lymph nodes (MLNs) are unknown. AIM To examine the expression of FasL on MLN DC during acute colitis. METHODS Acute colitis was induced in Sprague Dawley rats by administration of trinitrobenzene sulfonic acid (TNBS i.c.). At 72 hours the rats were sacrificed and the colons removed and scored for macroscopic damage. The cecum and small intestine were exteriorized and the MLN chain identified. After dissection of overlying mesenteric fat, the MLN were removed. The lymph nodes adjacent to the cecum were also removed. Isolation of DC and phenotypic characterization of FasL expression were performed by flow cytometry. RESULTS Animals receiving TNBS had significantly higher damage scores than untreated animals (p<0.0001). Expression of FasL on MLN DC was significantly higher in colitis animals (83%) than in controls (38% p<0.05). CONCLUSION Our results suggest that loss of FasL expression on MLN DC may be one of the mechanisms that contribute to the inappropriate apoptosis and subsequent T cell accumulation that occurs in IBD. Supported by 5F31DK077584.