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Cytokine Imbalance (cytokine + imbalance)
Selected AbstractsInflammatory Cytokine Imbalance after Coronary Angioplasty: Links with Coronary AtherosclerosisJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2007NATALE DANIELE BRUNETTI M.D., Ph.D. Aim:To investigate release of some inflammatory cytokines (Cys) after coronary angioplasty and its links with coronary atherosclerosis. Methods:Twenty-seven consecutive subjects with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI) were enrolled in the study: serial blood samples were taken in order to evaluate plasma concentrations of Interleukin (IL)-2, IL-10, IL-18, TNF,, and IFN, just before PCI at 12 and 24 hours. Patients were then divided, considering balance between each inflammatory Cy and IL-10, an antiinflammatory Cy, into four groups, ranging from a prevalent antiinflammatory response (stable inflammatory Cy,increasing IL-10 values) to a marked inflammatory imbalance (increasing inflammatory Cy,stable IL-10 values). Results:All Cys showed significant increases in plasma concentrations if compared with baseline values. Release curves were not significantly different when comparing subjects with ST-elevation myocardial infarction (STEMI) versus unstable angina,non-STEMI (UA-NSTEMI), diabetics versus controls. Subjects with marked inflammatory response showed a higher incidence of stenosis on left anterior descending (LAD) coronary artery (IL-2 ,2 and IFN, P < 0.05); Cy release was higher in patients with multivessel coronary disease (IL-2 and IFN,, ANOVA P < 0.01). Correlations were also referable between Cys and myocardial enzyme release. Subjects treated with sirolimus-eluting stents (SES) showed significantly lower Cy periprocedure ratio if compared with those treated with bare metal stents. Conclusions:A significant Cy release is detectable after PCI: inflammatory response seems to correlate with both PCI due to plaque instabilization and coronary atherosclerosis. A blunted inflammatory response is detectable in subjects treated with SES. [source] Effect of H1 -receptor antagonists on proliferative response, cytokine production, and cellular migration of human T cells and macrophagesCLINICAL & EXPERIMENTAL ALLERGY REVIEWS, Issue 2 2008S. Iwata Summary Cytokine imbalance and cellular migration to inflammatory sites are critical components of allergic diseases. Redirecting cytokine imbalance and inhibiting cell migration therefore represent important therapeutic strategies for the treatment of these disorders. We studied the in vitro effect of the non-sedating H1 -receptor antagonists ebastine, carebastine, epinastine, cetirizine, and ketotifen on cytokine secretion by human T cells under various co-stimulatory conditions and the migratory activity of activated T cells as well as production of pro-inflammatory cytokines by macrophages. Ebastine and carebastine inhibited T cell proliferation and production of IL-4, IL-5, IL-6, and TNF-, by T cells under co-stimulation with CD28 plus CD3, CD26 plus CD3, and CD3 plus phorbol myristate acetate, whereas these drugs had no effect on the production of IL-2 and IFN-,. Ebastine and carebastine also inhibited T cell migration and production of TNF-, and IL-6 by macrophages. Epinastine inhibited T cell proliferation and production of IL-2, IFN-,, IL-4, and IL-5, whereas it elicited no effect on the production of IL-6 and TNF-, by T cells and macrophages as well as T cell migration. Cetirizine and ketotifen had no effects on cytokine production and T cell migration. Our results suggest that certain H1 -receptor antagonists, most notably ebastine and carebastine, can influence T cell migration and cytokine production in addition to antagonizing the H1 receptor. These drugs therefore might be useful against T cell-mediated allergic inflammatory disorders such as asthma, atopic dermatitis, and psoriasis. [source] Signal transducers and activators of transcription 3 signaling pathway.INFLAMMATORY BOWEL DISEASES, Issue 2 2005An Essential Mediator of Inflammatory Bowel Disease, Other Forms of Intestinal Inflammation Abstract Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of chronic inflammatory bowel disease (IBD), are characterized by mucosal immune cell activation that is driven by a cytokine imbalance. Several cytokines involved in IBD act through the activation of the signal transducers and activators of transcription (STAT) family. We investigated the activation of STAT3 in the mucosa of CD and UC patients, and evaluated whether this event is specific for IBD patients. Using immunofluorescence and immunoblotting, total and phosphorylated STAT3 levels were assessed in biopsy specimens, isolated lamina propria mononuclear cells, and peripheral blood mononuclear cells from patients with CD, UC, other forms of intestinal inflammation, and control subjects. Immunoblotting revealed phosphorylated STAT3 in mucosal biopsy specimens from patients with CD, UC, celiac disease, and acute self-limited colitis, but not in the normal mucosa of control subjects. In IBD patients, STAT3 activation was confined to actively inflamed areas. Accordingly, activated STAT3 was detected in isolated lamina propria mononuclear cells from inflamed IBD tissues, but not in peripheral blood mononuclear cells from control subjects or IBD patients. Immunofluorescence demonstrated that the sources of activated STAT3 were macrophages and T lymphocytes, but not neutrophils. STAT3 activation also was detected in T cells infiltrating the duodenal mucosa of celiac disease patients. We conclude that STAT3 signaling occurs in both CD and UC, where it is strictly confined to areas of active inflammation and is limited to infiltrating macrophages and T cells. The occurrence of STAT3 signaling in other acute and chronic intestinal inflammatory conditions suggests that, rather than a specific feature of IBD, it represents a fundamental signaling pathway that is shared by multiple forms of gut inflammation. [source] T-helper 1/T-helper 2 cytokine imbalance and clinical phenotypes of acute-phase major depressionPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 4 2007TIAO-LAI HUANG md Abstract Several studies have discussed the relationships between T-helper 1 (Th1) or Th2 cytokines and major depression. The aim of the present study was to investigate the relationships between Th1/Th2 cytokine balance and clinical phenotypes of acute-phase major depression. A total of 82 subjects including 42 patients with major depressive disorder and 40 healthy controls were recruited. Serum cytokine levels of interleukin-1, (IL-1,), tumor necrosis factor-, (TNF-,) and IL-10 were examined. Using ancova with age and body mass index (BMI) adjustments, there were no significant differences in serum IL-1,, TNF-,, and IL-10 levels between patients with major depressive disorder and healthy controls. However, using ancova with BMI adjustment only, the results showed that patients with major depressive disorder had significantly higher TNF-, levels than control subjects. In addition, using ancova with age and BMI adjustments, significantly higher serum IL-1, level and IL-1,/IL-10 ratio were noted in patients with melancholic features than patients with non-melancholic features. However, there were no significant differences in serum IL-1,, TNF-, and IL-10 levels between patients with and without suicide attempt. In conclusion, serum TNF-,, IL-1, level and IL-1,/IL-10 ratio might play an important role in the psychopathology of acute-phase major depressive disorder. [source] Effect of H1 -receptor antagonists on proliferative response, cytokine production, and cellular migration of human T cells and macrophagesCLINICAL & EXPERIMENTAL ALLERGY REVIEWS, Issue 2 2008S. Iwata Summary Cytokine imbalance and cellular migration to inflammatory sites are critical components of allergic diseases. Redirecting cytokine imbalance and inhibiting cell migration therefore represent important therapeutic strategies for the treatment of these disorders. We studied the in vitro effect of the non-sedating H1 -receptor antagonists ebastine, carebastine, epinastine, cetirizine, and ketotifen on cytokine secretion by human T cells under various co-stimulatory conditions and the migratory activity of activated T cells as well as production of pro-inflammatory cytokines by macrophages. Ebastine and carebastine inhibited T cell proliferation and production of IL-4, IL-5, IL-6, and TNF-, by T cells under co-stimulation with CD28 plus CD3, CD26 plus CD3, and CD3 plus phorbol myristate acetate, whereas these drugs had no effect on the production of IL-2 and IFN-,. Ebastine and carebastine also inhibited T cell migration and production of TNF-, and IL-6 by macrophages. Epinastine inhibited T cell proliferation and production of IL-2, IFN-,, IL-4, and IL-5, whereas it elicited no effect on the production of IL-6 and TNF-, by T cells and macrophages as well as T cell migration. Cetirizine and ketotifen had no effects on cytokine production and T cell migration. Our results suggest that certain H1 -receptor antagonists, most notably ebastine and carebastine, can influence T cell migration and cytokine production in addition to antagonizing the H1 receptor. These drugs therefore might be useful against T cell-mediated allergic inflammatory disorders such as asthma, atopic dermatitis, and psoriasis. [source] Relationship of in vivo and ex vivo levels of TH1 and TH2 cytokines with viremia in HAART patients with and without opportunistic infectionsJOURNAL OF MEDICAL VIROLOGY, Issue 4 2006Sardar Sindhu Abstract TH1/TH2 cytokines' imbalance is critical to HIV-1 progression and pathogenesis. Opportunistic infections-related cytokine perturbations in the setting of highly active antiretroviral therapy (HAART) are unclear. The objective of this cross-sectional study was to identify the relationship between TH1/TH2 cytokines and viremia in HAART patients with/without opportunistic infections. Sera from 17 HAART patients with and 43 without opportunistic infections, and 20 HIV-seronegative controls were used to measure the levels of IL-2, IFN-,, IL-4, and IL-10 proteins and mRNAs by ELISA and RNase protection assays, respectively. Ex vivo cytokine production by the CD4+/CD8+ T cells from four low and four high viremia patients randomly selected from non-opportunistic infection group was also evaluated. Serum IL-2 and IFN-, levels were lower (P,<,0.05) in patients than controls; this reduction was more pronounced for IFN-, in non-opportunistic infection patients. IL-4 and IL-10 were higher in patients than controls; this elevation was more remarkable in patients with opportunistic infections. Serum TH1/TH2 cytokine levels correlated with viremia. In vitro cytokine production assays showed that CD4+ T cells from low viremia patients mainly produced IL-2 and IFN-,, CD8+ T cells from high viremia patients produced IL-4, and both subsets comparably produced IL-10 in patients with similar viremia. Positive correlations between sera/supernatant proteins and cellular mRNAs were also found statistically significant (P,<,0.05). It was therefore concluded that in vivo TH1/TH2 cytokine levels in HAART patients and their ex vivo production by the CD4+/CD8+ T cells correlated with viremia and were also modulated by the presence of opportunistic infections in these patients. J. Med. Virol. 78:431,439, 2006. © 2006 Wiley-Liss, Inc. [source] |