Involvement of CD4+ T Cells in the Development of Dextran Sulfate Sodium-Induced Experimental Colitis and Suppressive Effect of IgG on Their Action

Shintani, Nahoko; Nakajima, Tsunetaka; Okamoto, Takeaki; Kondo, Takao; Nakamura, Norifumi; Mayumi, Tadanori

doi:10.1016/s0306-3623(98)00004-4

Cited by 56 publications

(44 citation statements)

References 21 publications

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“…These results confirmed our earlier findings that the numbers of CD4 ϩ T cells in spleens, MLN, and LP represent the majority of lymphocytes expressing inflammatory cytokines during colitis (Singh et al, 2008a). This finding is also in agreement with the findings of other studies using DSS-induced colitis models that showed the potentiation of CD4 ϩ T cells in colitis (Dieleman et al, 1998;Shintani et al, 1998;Grose et al, 2001;Ogawa et al, 2004). The present results imply that intestinal inflammation is driven by the presence of CD4 ϩ T cells and potentiated by Th1 and inflammatory cytokines, which can be abrogated by resveratrol treatment.…”

Section: Fig 8 Resveratrol Modulates Dss-induced Cd4supporting

confidence: 93%

Resveratrol (Trans-3,5,4′-trihydroxystilbene) Induces Silent Mating Type Information Regulation-1 and Down-Regulates Nuclear Transcription Factor-κB Activation to Abrogate Dextran Sulfate Sodium-Induced Colitis

Singh

Singh²,

Singh³

et al. 2009

J Pharmacol Exp Ther

184

172

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Inflammatory bowel disease is a chronic, relapsing, and tissuedestructive disease. Resveratrol (3,4,5-trihydroxy-trans-stilbene), a naturally occurring polyphenol that exhibits beneficial pleiotropic health effects, is recognized as one of the most promising natural molecules in the prevention and treatment of chronic inflammatory disease and autoimmune disorders. In the present study, we investigated the effect of resveratrol on dextran sodium sulfate (DSS)-induced colitis in mice and found that it effectively attenuated overall clinical scores as well as various pathological markers of colitis. Resveratrol reversed the colitis-associated decrease in body weight and increased levels of serum amyloid A, tumor necrosis factor-␣, interleukin (IL-6), and IL-1␤. After resveratrol treatment, the percentage of CD4 ϩ T cells in mesenteric lymph nodes (MLN) of colitis mice was restored to normal levels, and there was a decrease in these cells in the colon lamina propria (LP). Likewise, the percentages of macrophages in MLN and the LP of mice with colitis were decreased after resveratrol treatment. Resveratrol also suppressed cyclooxygenase-2 (COX-2) expression induced in DSS-exposed mice. Colitis was associated with a decrease in silent mating type information regulation-1 (SIRT1) gene expression and an increase in p-inhibitory B expression and nuclear transcription factor-B (NF-B) activation. Resveratrol treatment of mice with colitis significantly reversed these changes. This study demonstrates for the first time that SIRT1 is involved in colitis, functioning as an inverse regulator of NF-B activation and inflammation. Furthermore, our results indicate that resveratrol may protect against colitis through up-regulation of SIRT1 in immune cells in the colon.

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Section: Fig 8 Resveratrol Modulates Dss-induced Cd4supporting

confidence: 93%

Resveratrol (Trans-3,5,4′-trihydroxystilbene) Induces Silent Mating Type Information Regulation-1 and Down-Regulates Nuclear Transcription Factor-κB Activation to Abrogate Dextran Sulfate Sodium-Induced Colitis

Singh

Singh²,

Singh³

et al. 2009

J Pharmacol Exp Ther

184

172

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“…Although it is reported that DSS colitis can be induced in lymphocyte deficient SCID mice, Kim et al have shown that lymphocytes are involved in the onset of DSS colitis by the fact that disease progression was slower in lymphocyte deficient Rag-1 KO mice compared to the wild type C57BL/6 mice (55-57). Furthermore, a chronic form of DSS induced colitis has been shown to have a T cell component (58). Hence it is conceivable that DSS induced colitis is modulated more effectively by CD5 deficient T reg cells.…”

Section: Discussionmentioning

confidence: 99%

CD5 plays an inhibitory role in the suppressive function of murine CD4+ CD25+ Treg cells

et al. 2008

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A subset of CD4 + T cells, the CD4 + CD25 + T reg cells in the lymphoid organs and peripheral blood are known to possess suppressive function. Previous in vitro and in vivo studies have indicated that T cell receptor (TCR) signal is required for development of such 'natural regulatory (T reg ) cells' and for activation of the effector function of CD4 + CD25 + regulatory T cells. CD5 is a cell surface molecule present on all T cells and a subtype of B lymphocytes, the B-1 cells, primarily localized to coelomic cavities, Peyer's patches, tonsils and spleen. CD5 acts as a negative regulator of T cell and B cell signaling via recruitment of SHP-1. Here, we demonstrate that T reg cells obtained from CD5 −/− mice are more potent than those from wild type mice in suppressing the in vitro cell proliferation of anti-CD3 stimulated CD4 + CD25 − responder T cells. This phenomenon was cell contact and GITR dependent. Lack of CD5 expression on T reg cells (from spleen, lymph node and thymus) did not affect the intracellular levels of Foxp3. However, CD5 −/− T reg thymocytes were able to elicit a higher Ca 2+ response to TCR + co-stimulatory signals than the wild type cells. CD5 −/− mice expressed more Foxp3 mRNA in the colon than wild type mice, and additionally, the severity of the DSS-induced colitis in CD5 −/− mice was less than the wild type strain. We suggest that manipulation of CD5 expression or the downstream signaling components of CD4 + CD25 + T reg cells as a potential strategy for therapeutic intervention in cases of auto-immune disorders.

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“…Lymphocytes are not required for induction of acute DSS colitis, since the disease can be induced in SCID mice (Dieleman et al, 1994). The chronic model, however, may be governed by interactions of macrophages with T cells Shintani et al, 1998;Leung et al, 2000). It is intriguing to note that the immunosuppressant cyclosporin exacerbated acute DSS colitis when administered prophylactically, yet was beneficial if given therapeutically or during the chronic phase of DSS colitis.…”

Section: Discussionmentioning

confidence: 99%

Antisense Oligonucleotide Blockade of Tumor Necrosis Factor-α in Two Murine Models of Colitis

Myers

Murthy²,

Flanigan³

et al. 2003

J Pharmacol Exp Ther

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Tumor necrosis factor-␣ (TNF-␣) is a key cytokine involved in the pathogenesis of inflammatory bowel disease. We have developed a second-generation antisense oligonucleotide (ISIS 25302) specific for murine TNF-␣ and have evaluated this oligonucleotide in two models of gut inflammation of distinct etiology. ISIS 25302 decreased TNF-␣ mRNA in a dose-and sequence-dependent manner in vitro in the mouse macrophage cell line P388D1. It also reduced TNF-␣ mRNA in vivo, in whole adipose tissue and in macrophages isolated from the adipose tissue of db/db mice, a strain with constitutively high expression of TNF-␣. ISIS 25302 significantly reduced disease activity index scores in mice with both an acute and a chronic form of dextran sodium sulfate (DSS)-induced colitis. It also significantly improved histopathological scores in interleukin (IL)-10-deficient mice. This was accompanied by reductions in both the basal and lipopolysaccharide-stimulated secretion of TNF-␣ and interferon-␥ in colonic organ cultures from IL-10 Ϫ/Ϫ mice. In this model, efficacy was obtained with both a prophylactic treatment regimen or a therapeutic dosing protocol begun after colitis was already present. In both the DSS and IL-10 Ϫ/Ϫ models, scrambled and mismatch control oligonucleotides were largely without effect, suggesting that ISIS 25302 was exerting its effects through a sequence-dependent antisense mechanism.

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Involvement of CD4+ T Cells in the Development of Dextran Sulfate Sodium-Induced Experimental Colitis and Suppressive Effect of IgG on Their Action

Cited by 56 publications

References 21 publications

Resveratrol (Trans-3,5,4′-trihydroxystilbene) Induces Silent Mating Type Information Regulation-1 and Down-Regulates Nuclear Transcription Factor-κB Activation to Abrogate Dextran Sulfate Sodium-Induced Colitis

Resveratrol (Trans-3,5,4′-trihydroxystilbene) Induces Silent Mating Type Information Regulation-1 and Down-Regulates Nuclear Transcription Factor-κB Activation to Abrogate Dextran Sulfate Sodium-Induced Colitis

CD5 plays an inhibitory role in the suppressive function of murine CD4+ CD25+ Treg cells

Antisense Oligonucleotide Blockade of Tumor Necrosis Factor-α in Two Murine Models of Colitis

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