The inflammatory infiltrate in the acute stage of the dextran sulphate sodium induced colitis: B cell response differs depending on the percentage of DSS used to induce it

Abstract

BackgroundExperimental colitis with features similar to inflammatory bowel disease (IBD) has initially been described. A detailed analysis of inflammatory cells has not yet been described. Therefore in this study we characterized the cells involved in the acute phase of the colitis and compared those findings to what is known about human IBD.MethodsColitis was induced in BALB/C and C57Bl6 mice by ingestion of 2.5% and 5% DSS in the drinking water for 8 days. Cells were labelled by immunohistochemical staining with F4/80 and ER-MP20 for macrophages, TIB 120 for MHC Class II presentation, and anti-CD4 and anti-CD8 antibodies. They were enumerated by using a novel method that employs video image analysis. Immunoglobulin-producing cells were enumerated by immunofluorescent staining for IgA, IgG and IgM and counting by using confocal microscopy.ResultsInflammatory infiltrate in the acute phase of the dextran sulphate sodium (DSS) -induced colitis consists predominantly of macrophages, neutrophils and eosinophils. Neutrophils increase in numbers and crypt abscesses were also seen. Increased macrophage numbers were due to recently recruited monocytes from the peripheral circulation. It does not appear that there are any changes in T cell numbers or distribution. The inflammation induced changes in immunoglobulin-producing cells with IgA-producing cells affected the most.ConclusionsThe effect on Ig-producing cells depends on the percentage of DSS used to induce colitis. In general, 2.5% DSS induces an increase and 5% DSS a depletion of these cells.

C-Type Lectin SIGN-R1 Has a Role in Experimental Colitis and Responsiveness to Lipopolysaccharide

“…In the colitis model used in this study, DSS, a sulfated polymer, induces intestinal injury by a direct toxic effect on epithelial cells of the basal crypt, with a loss of integrity in the mucosal barrier allowing infiltration of intestinal bacteria (21). Subsequently, colon inflammation develops with an infiltration of macrophages, neutrophils, and eosinophils into the colon and increased production of the inflammatory cytokines IL-1b, TNF-a, and IL-6, which contribute to the inflammation and damage to the colon (21,31). In this study, the severity of all DSS-induced pathology was significantly reduced in SIGN-R1 2/2 mice relative to wild-type animals, suggesting that recognition of bacterial surface carbohydrates by SIGN-R1 may contribute to the development of intestinal inflammation.…”

Regulation of dextran sodium sulfate induced colitis by leukocyte beta 2 integrins

“…Previous reports have implicated a role for B cells during DSS colitis, yet the true pathological importance of this cell population during experimental colitis remains poorly understood. 58,59 CD11b may be important for B-cell function and/or recruitment. We have recently reported that the loss of CD11b in the MRL/ MpJ-Fas lpr mouse lupus model results in enhanced lymphadenopathy with focal accumulation of plasma and Mott cells.…”

Interleukin 6 inhibition by triptolide prevents inflammation in a mouse model of ulcerative colitis

“…According to the method by Stevceva et al (28) from 2001, a mouse model of UC was established using dextran sulfate sodium (DSS; MP Biomedicals, Santa Ana, CA, USA). A total of 80 female BALB/c mice were stochastically divided into eight groups and housed in separate cages (10 mice per cage).…”