Correlation of Serum Soluble TNF-alpha Receptors I and II Levels with Disease Activity in Patients with Ulcerative Colitis

Hanai, Hiroyuki; Watanabe, Fumio; Yamada, Masami; Sato, Yoshihiko; Takeuchi, Ken; Iida, Takayuki; Tozawa, Kotaro; Tanaka, Tatsuo; Maruyama, Yasuhiko; Matsushita, Ikumi; Iwaoka, Yasushi; Saniabadi, Abby R.

doi:10.1111/j.1572-0241.2004.30432.x

Cited by 67 publications

(49 citation statements)

References 53 publications

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“…Single platelets were gated to a separate scatter plot and FITC-fluorescence threshold was determined using isotypic-matched controls. Platelets with FITC-fluorescence from anti-CD62P above this threshold were considered activated [15][16][17].…”

Section: Flow Cytometric Analysismentioning

confidence: 99%

Increased circulating platelet–neutrophil, platelet–monocyte complexes, and platelet activation in patients with ulcerative colitis: A comparative study

et al. 2006

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It is reported that the incidence of thromboembolism is increased in ulcerative colitis (UC), and hypercoagulability persists even when patients are in remission. We evaluated the association of inflammatory response parameters with UC activity, and activation parameters of the platelets, endothelium, and the coagulation system in UC. Eighteen UC patients and 19 healthy subjects were included in the study. The patients' clinical features were recorded down; whole blood counts and acute phase parameters were evaluated. UC patients were divided into two as active (9 patients) and inactive (9 patients) according to combined clinical activity index (CAI) and endoscopic activity index (EAI) scores. In all subjects, platelet CD62P expression, platelet-monocyte complexes (PMC), platelet-neutrophil complexes (PNC), and platelet microparticles (PMP) were determined by flow cytometry. E-selectin, thrombin-antithrombin complex (TAT) levels in plasma, and sCD40L levels in serum were determined by ELISA. In both active and inactive UC patients, platelet CD62P expression, the percentages of PMC, and PNC were significantly higher than those in the control group (P < 0.01). PMP level was higher in the control group than in inactive UC patients (P = 0.001). sCD40L level was significantly higher in active UC group than in the control group (P < 0.01). EAI score correlated significantly with PMP (r = 0.5, P = 0.04) and sCD40L (r = 0.48, P = 0.044); CAI score had a negative correlation (r = -0.68, P = 0.002) with sE-selectin level. In addition to increased CD62P expression and sCD40L, increased formation of PMC and PNC suggests a role for plateletleukocyte complex formation together with platelet activation in thromboembolic events observed in UC. Am. J. Hematol. 81:753-759, 2006. V V C 2006 Wiley-Liss, Inc.

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Section: Flow Cytometric Analysismentioning

confidence: 99%

Increased circulating platelet–neutrophil, platelet–monocyte complexes, and platelet activation in patients with ulcerative colitis: A comparative study

et al. 2006

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“…Apart from its importance in host defense, the migration of neutrophils to inflammatory sites is, at least in part, responsible for the tissue damage observed in several autoimmune inflammatory diseases, such as rheumatoid arthritis, glomerulonephritis, autoimmune vasculitis and inflammatory bowel disease [3][4][5]. The migration of neutrophils from the blood into the affected tissues depends on a cascade of chemotactic mediators, especially chemokines, triggered by activation of cells resident in the inflamed area [6,7].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil recruitment in immunized mice depends on MIP‐2 inducing the sequential release of MIP‐1α, TNF‐α and LTB₄

et al. 2006

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Neutrophils are thought to play an important role in the tissue damage observed in various autoimmune diseases. Chemokines, cytokines and leukotrienes have recognized roles in the orchestration of neutrophil migration. We have recently shown that antigeninduced neutrophil migration into the peritoneum of immunized mice is mediated by macrophage-inflammatory protein (MIP)-1a which interacts with CCR1 and induces the sequential release of TNF-a and leukotriene B 4 (LTB 4 ). The present study investigates the role of MIP-2 and CXCR2 in the cascade of events leading to mediator generation and neutrophil influx. Antigen challenge of immunized mice induced the expression of CXCR2 and the production of KC and MIP-2 proteins. Antigen-induced neutrophil migration was inhibited by a CXCR2 receptor antagonist (repertaxin) or an anti-MIP-2 antibody, but not by an anti-KC antibody. Administration of MIP-2 promoted a dose-dependent neutrophil migration in naive mice which was inhibited by repertaxin, anti-TNF-a, anti-MIP-1a antibodies or by MK886 (leukotriene synthesis inhibitor). MIP-2 administration induced the release of MIP-1a, TNF-a and LTB 4 , and the release of the latter two was inhibited by anti-MIP-1a antibody treatment. Our studies highlight the intricate balance between mediator production and action during an immune-mediated inflammatory response and suggest a mediator cascade leading to neutrophil influx following antigen challenge of immunized mice: MIP-2 ? MIP-1a ? TNF-a ? LTB 4 .

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“…Similarly, TNF-α levels in stool samples from patients with active UC were signifi cantly increased compared with healthy controls (Braegger et al 1992). Serum levels of TNF-α and TNFR were also shown to be signifi cantly higher in UC patients than those of healthy controls and their levels were shown to correlate with disease activity (Komatsu et al 2001;Hanai et al 2004;Spoettl et al 2007).…”

Section: Role Of Tnf-α In Ulcerative Colitismentioning

confidence: 99%

Infliximab in ulcerative colitis

Levin

Shibolet²

2008

BTT

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Infl iximab, a monoclonal anti-TNF-α antibody, is commonly used for treatment of moderate to severe Crohn's disease (CD). Its role in the treatment for ulcerative colitis (UC) remains controversial. We review the role of TNF-α in the pathogenesis of UC and describe the randomized, double-blind, placebo-controlled trials and systematic reviews that assess the effi cacy of infl iximab in the treatment of moderate to severe UC.

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Correlation of Serum Soluble TNF-alpha Receptors I and II Levels with Disease Activity in Patients with Ulcerative Colitis

Abstract: The sources of s-RI/RII are believed to be activated monocytes and neutrophils with further release when these leukocytes adhere to the column carriers. s-RI/RII released during GMA should contribute to the clinical efficacy of this procedure.

Cited by 67 publications

References 53 publications

Increased circulating platelet–neutrophil, platelet–monocyte complexes, and platelet activation in patients with ulcerative colitis: A comparative study

Increased circulating platelet–neutrophil, platelet–monocyte complexes, and platelet activation in patients with ulcerative colitis: A comparative study

Neutrophil recruitment in immunized mice depends on MIP‐2 inducing the sequential release of MIP‐1α, TNF‐α and LTB₄

Infliximab in ulcerative colitis

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Correlation of Serum Soluble TNF-alpha Receptors I and II Levels with Disease Activity in Patients with Ulcerative Colitis

Abstract: The sources of s-RI/RII are believed to be activated monocytes and neutrophils with further release when these leukocytes adhere to the column carriers. s-RI/RII released during GMA should contribute to the clinical efficacy of this procedure.

Cited by 67 publications

References 53 publications

Increased circulating platelet–neutrophil, platelet–monocyte complexes, and platelet activation in patients with ulcerative colitis: A comparative study

Increased circulating platelet–neutrophil, platelet–monocyte complexes, and platelet activation in patients with ulcerative colitis: A comparative study

Neutrophil recruitment in immunized mice depends on MIP‐2 inducing the sequential release of MIP‐1α, TNF‐α and LTB4

Infliximab in ulcerative colitis

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Neutrophil recruitment in immunized mice depends on MIP‐2 inducing the sequential release of MIP‐1α, TNF‐α and LTB₄