Cytokines (Immunoinflammatory Hormones) and Their Natural Regulation in Inflammatory Bowel Disease (Crohn’s Disease and Ulcerative Colitis): A Review

Brynskov, Jørn; Nielsen, Ole Haagen; Ahnfelt-Rønne, I.; Bendtzen, Klaus

doi:10.1159/000171464

Cited by 71 publications

(40 citation statements)

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“…[2][3][4] The local production of tumor necrosis factor a (TNF-a ) is thought to have a key role in the initiation and propagation of Crohn's disease. [5][6][7] Production of TNF-a in the intestinal mucosa is increased in patients with Crohn's disease. [7][8][9] Neutralization of TNF-a has been suggested as a therapeutic intervention in inflammatory diseases, such as inflammatory bowel disease and rheumatoid arthritis.…”

Section: Discussionmentioning

confidence: 99%

Infliximab for the Treatment of Fistulas in Patients with Crohn's Disease

Rutgeerts²,

et al. 1999

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Section: Discussionmentioning

confidence: 99%

Infliximab for the Treatment of Fistulas in Patients with Crohn's Disease

Rutgeerts²,

et al. 1999

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“…However, the diminished IFN-␥ and increased IL-10 expression observed in the CCR2-deficient mice may have been sufficient to decrease attenuate the severity of the colonic damage by reducing macrophage inflammatory function (54). The proinflammatory role of IFN-␥ in the activation of macrophages in animal models of IBD and in Crohn's disease has been well established (55,63). IL-10 is able to reduce macrophage secretion of inflammatory mediators by directly inhibiting NF-B activation (64).…”

Section: Discussionmentioning

confidence: 99%

Mice with a Selective Deletion of the CC Chemokine Receptors 5 or 2 Are Protected from Dextran Sodium Sulfate-Mediated Colitis: Lack of CC Chemokine Receptor 5 Expression Results in a NK1.1+ Lymphocyte-Associated Th2-Type Immune Response in the Intestine

Andres¹,

Beck²,

Mizoguchi

et al. 2000

The Journal of Immunology

231

152

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The chemokine receptors CCR2 and CCR5 and their respective ligands regulate leukocyte chemotaxis and activation. To determine the role of these chemokine receptors in the regulation of the intestinal immune response, we induced colitis in CCR2- and CCR5-deficient mice by continuous oral administration of dextran sodium sulfate (DSS). Both CCR2- and CCR5-deficient mice were susceptible to DSS-induced intestinal inflammation. The lack of CCR2 or CCR5 did not reduce the DSS-induced migration of macrophages into the colonic lamina propria. However, both CCR5-deficient mice and, to a lesser degree, CCR2-deficient mice were protected from DSS-induced intestinal adhesions and mucosal ulcerations. CCR5-deficient mice were characterized by a greater relative infiltration of CD4+ and NK1.1+ lymphocyte in the colonic lamina propria when compared to wild-type and CCR2-deficient mice. In CCR5-deficient mice, mucosal mRNA expression of IL-4, IL-5, and IL-10 was increased, whereas that of IFN-γ was decreased, corresponding to a Th2 pattern of T cell activation. In CCR2-deficient mice, the infiltration of Th2-type T cells in the lamina propria was absent, but increased levels of IL-10 and decreased levels of IFN-γ may have down regulated mucosal inflammation. Our data indicate that CCR5 may be critical for the promotion of intestinal Th1-type immune responses in mice.

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“…IBD is represented by two specific gastrointestinal disorders: ulcerative colitis (UC) and Crohn's disease (CD), both of them characterized by chronic inflammatory processes. Although etiology and pathogenesis of IBD are still unknown, there is evidence that proinflammatory cytokines like interleukin-1β (IL1β) and interleukin-6 (IL6) are involved in the establishment of IBD [16,17]. IL1β and IL6 mRNA were found in large numbers of cells throughout the inflamed intestine of patients with CD but also in some macroscopically unaffected tissue specimens of the same patients [18].…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of <i>TFF</i> Expression in Gastrointestinal Cell Lines by Cytokines and Nuclear Factors

Dossinger¹,

Kayademir²,

Blin³

et al. 2002

Cell Physiol Biochem

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Background and Aims: Trefoil peptides (TFF1, TFF2 and TFF3) are acute phase proteins up-regulated in response to gastrointestinal mucosal damage. They promote cell migration, protect and heal the mucosa and may function as tumorsuppressors. We assumed them to be regulated by the proinflammatory cytokines interleukin-1β (IL1β) and interleukin-6 (IL6), which trigger the transcriptional factors NF-ĸB and C/EBPβ. Methods: Following IL1β and IL6 stimulation, expression of TFF genes was analyzed in gastrointestinal cell lines HT-29 and KATO III by reporter gene assays using TFF promoter constructs and by quantitative real-time PCR. NF-ĸB and C/EBPβ were transiently co-expressed. Results: We have functionally identified transcription factors NF-ĸB and C/EBPβ to inhibit transcription of human TFF genes. Down-regulation of TFF transcription is also observed by IL1β and IL6, suggesting crosstalk with or in response to the immune system. IL1β and IL6 caused a 3- to 11-fold reduction in TFF mRNA expression, displayed in real-time PCR. Conclusions: Down-regulation of intestinal trefoil factor TFF3 due to transcriptional repression by IL1β through NF-ĸB as well as by IL6 through C/EBPβ activation in vitro may reflect the situation in vivo and may contribute to ulceration and decreased wound healing during inflammatory bowel disease. Additionally, IL1 and IL6 over-expression in chronic gastritis may lead to mucosal damage and gastric carcinogenesis through transcriptional repression of TFF1 and TFF2.

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Cytokines (Immunoinflammatory Hormones) and Their Natural Regulation in Inflammatory Bowel Disease (Crohn’s Disease and Ulcerative Colitis): A Review

Cited by 71 publications

References 0 publications

Infliximab for the Treatment of Fistulas in Patients with Crohn's Disease

Infliximab for the Treatment of Fistulas in Patients with Crohn's Disease

Mice with a Selective Deletion of the CC Chemokine Receptors 5 or 2 Are Protected from Dextran Sodium Sulfate-Mediated Colitis: Lack of CC Chemokine Receptor 5 Expression Results in a NK1.1+ Lymphocyte-Associated Th2-Type Immune Response in the Intestine

Down-regulation of <i>TFF</i> Expression in Gastrointestinal Cell Lines by Cytokines and Nuclear Factors

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