Elevated cell‐associated levels of interleukin 1β and interleukin 6 in inflamed mucosa of inflammatory bowel disease

Gröttrup-Wolfers, E; Møeller, Jesper Bonnet; Karbach, U.; Müller-Lissner, S; Endres, Stefan

doi:10.1046/j.1365-2362.1996.123262.x

Cited by 30 publications

(15 citation statements)

References 34 publications

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“…In support of the above, substantially higher amounts of circulating IL-6 have been found in patients with CD compared with controls [4,6] . To further investigate the involvement of IL-6 signaling in colitis, Ito et al [7] treated mice with anti-IL-6 receptor monoclonal antibody subjected to different experimental models of chronic colitis.…”

Section: Il-6 Genetic Ablation Protects From Tnbs-induced Colitis In supporting

confidence: 58%

Interleukin-6 Genetic Ablation Protects from Trinitrobenzene Sulfonic Acid-Induced Colitis in Mice

Gay

Kokkotou

O’Brien

et al. 2006

Neuroimmunomodulation

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Background: Interleukin (IL)-6 is a proinflammatory cytokine implicated in the pathogenesis of inflammatory bowel disease. IL-6 is locally upregulated in inflammatory bowel disease patients and in murine models of experimental colitis. Treatment with anti-IL-6 receptor antibody ameliorates intestinal inflammation. Objective: It was the aim of this study to investigate the role of genetic IL-6 deficiency in trinitrobenzene sulfonic acid (TNBS)-mediated colitis, an experimental model inflammation that shares several features with Crohn’s disease in humans. Methods: Acute colitis was induced in wild-type and IL-6-deficient (Il-6^–/–) mice by intracolonic administration of TNBS. Forty-eight hours after treatment, the local and systemic features of inflammation, i.e. food intake, weight loss, histological markers of colitis, cytokine expression by real-time PCR, food intake and body weight changes, were assessed. Results: In wild-type mice, TNBS administration increased both IL-6 serum levels and local expression of IL-6 by 36 and 9 fold, respectively, compared with control, vehicle-injected mice. Compared with the wild-type mice, the Il-6^–/– mice had significantly reduced intestinal inflammation as evidenced by epithelial damage, neutrophil infiltration, colon thickness and proinflammatory cytokine expression, following treatment with TNBS. Moreover, baseline levels of the antiinflammatory cytokines IL-10 and tumor growth factor-β were significantly elevated in Il-6^–/–compared with the wild-type mice. Conclusions: Our results demonstrate that Il-6^–/–are partially protected from the development of TNBS-induced acute experimental colitis, most likely via their significantly elevated baseline levels of antiinflammatory cytokines.

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Section: Il-6 Genetic Ablation Protects From Tnbs-induced Colitis In supporting

confidence: 58%

Interleukin-6 Genetic Ablation Protects from Trinitrobenzene Sulfonic Acid-Induced Colitis in Mice

Gay

Kokkotou

O’Brien

et al. 2006

Neuroimmunomodulation

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“…These results suggest a possible role for these cytokines in the colonic inflammatory state. Other investigators have found a correlation between severity of inflammation and pro-inflammatory cytokine levels in the colon of patients with inflammatory bowel disease and in animal models of colitis (Braegger et al, 1992;Brown et al, 2002;Carty et al, 2000;Dieleman et al, 1996;Grottrup-Wolfers et al, 1996).…”

Section: Discussionmentioning

confidence: 94%

Localized colonic inflammation increases cytokine levels in distant small intestinal segments in the rat

Barada¹,

Mourad²,

Sawah³

et al. 2006

Life Sciences

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“…Long-term treatment with steroids can improve growth by establishing equilibrium among IGFBPs favouring IGF bioactivity [7], but impair growth by inhibiting bone formation and GH secretion [8, 9]. In CD and ulcerative colitis (UC), interleukin (IL)-1β, IL-6 and tumour necrosis factor (TNF)-α may be increased in intestinal mucosal cells from collagenase-digested biopsies [10, 11], and from organ culture of biopsy specimens [12]. Serum concentrations of these cytokines may also be increased during clinical relapse [13, 14].…”

Section: Introductionmentioning

confidence: 99%

Relationships between Serum IGF-1, IGFBP-2, Interleukin-1Beta and Interleukin-6 in Inflammatory Bowel Disease

Street¹,

de’Angelis²,

Camacho‐Hübner

et al. 2004

Horm Res Paediatr

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Aims: To study the relationships between serum IGF-1, IGFBP-3 and IGFBP-2 and interleukin (IL)-1β and IL-6 in inflammatory bowel disease (IBD). Methods: Thirty-seven patients (18 males, 19 females, aged 8.8–26.1 years) with IBD (Crohn’s disease, CD, n = 17, and ulcerative colitis, UC, n = 20) were studied. Patients were in relapse or remission according to established criteria. Serum IGF-1, IGFBP-3, IGFBP-2, IL-1β and IL-6 levels were determined in patients and 15 healthy controls (aged 8.2–19.0 years). Results: IGF-1 levels were lower in patients with CD in relapse compared with controls (p < 0.05). IGFBP-2 levels were higher in CD in relapse compared with other groups (all p < 0.05). In CD and UC patients (n = 37), IGF-1 levels were inversely correlated with the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). IGFBP-2 levels correlated positively with ESR and IL-1β. IL-6 levels correlated positively with ESR and CRP. IL-1β levels were elevated in CD in relapse compared to controls (p < 0.05) and were higher in UC in relapse than in other groups (all p < 0.05). In combined CD/UC patients in relapse (n = 20), IL-1β levels were higher (p < 0.05) in patients with recto-sigmoiditis (n = 5) than in other patients. Conclusions: IGF-1, IGFBP-2 levels were related to IL levels, disease activity and anatomical distribution, consistent with active inflammation modifying the IGF-IGFBP system, possibly relevant to disturbance of growth.

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Elevated cell‐associated levels of interleukin 1β and interleukin 6 in inflamed mucosa of inflammatory bowel disease

Cited by 30 publications

References 34 publications

Interleukin-6 Genetic Ablation Protects from Trinitrobenzene Sulfonic Acid-Induced Colitis in Mice

Interleukin-6 Genetic Ablation Protects from Trinitrobenzene Sulfonic Acid-Induced Colitis in Mice

Localized colonic inflammation increases cytokine levels in distant small intestinal segments in the rat

Relationships between Serum IGF-1, IGFBP-2, Interleukin-1Beta and Interleukin-6 in Inflammatory Bowel Disease

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