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Circulating Interleukin (circulating + interleukin)
Selected AbstractsKinetics of host immune responses and cytomegalovirus resistance in a liver transplant patientLIVER TRANSPLANTATION, Issue 10 2009Kirsten Schaffer Among solid organ transplant (SOT) recipients, donor-seropositive/recipient-seronegative (D+/R,) cytomegalovirus (CMV) status is associated with the highest risk of ganciclovir-resistant CMV disease, which has been reported for patients receiving oral ganciclovir but not valganciclovir prophylaxis. We report a case of CMV breakthrough infection in a D+/R, liver transplant patient while he was receiving oral valganciclovir. Forty samples collected over 6 months were analyzed for the CMV viral load, lymphocyte counts, cytokine levels, and lymphocyte differentiation status. Genotypic resistance testing of the viral UL97 gene was performed when the patient failed to respond. CMV viremia occurred on day 50 post-transplant, and 5 samples taken between days 50 and 85 showed the wild-type UL97 genotype. The appearance of deletion 594-595 was observed from day 114 post-transplant. Viral loads declined when foscarnet was commenced and remained below 10,000 copies/mL when the lymphocyte count was greater than 1000/,L (P = 0.02). T cell responses revealed significant expansion of CD8+ terminal effector memory cells. CD4+ cells were largely populations of naïve and central memory cells. Circulating interleukin 10 (IL-10) levels correlated with the viral load (P < 0.0001). Seroconversion occurred on day 230. The CMV viral load in combination with lymphocyte counts and IL-10 may be a predictive marker for the risk of development of resistant CMV disease in D+/R, SOT patients. Liver Transpl 15:1199,1203, 2009. © 2009 AASLD. [source] Muscle Endurance in Elderly Nursing Home Residents Is Related to Fatigue Perception, Mobility, and Circulating Tumor Necrosis Factor-Alpha, Interleukin-6, and Heat Shock Protein 70JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 3 2008(See editorial comments by Drs. Hermes Florez, Bruce R. Troen, pp 55 OBJECTIVES: To explore the relationships between muscle endurance and circulating interleukin (IL)-6, tumor necrosis factor alpha (TNF-,), and heat shock protein (Hsp)70 in nursing home residents and to assess how muscle endurance relates to self-perceived fatigue and mobility. DESIGN: Exploratory study. SETTING: Three nursing homes of the Foundation for Psychogeriatrics (Brussels, Belgium). PARTICIPANTS: Seventy-seven residents (53 female and 24 male, mean age 81 ± 8). MEASUREMENTS: Participants were assessed for muscle endurance (fatigue resistance and grip work); perceived fatigue (visual analogue scale for fatigue); fatigue during daily activities (Mobility-Tiredness Scale); effect of fatigue on quality of life (World Health Organization Quality Of Life questionnaire); mobility (Tinetti Test & Elderly Mobility Scale (EMS)); and circulating IL-6, TNF-,, and Hsp70. RESULTS: Residents with better fatigue resistance reported less self-perceived tiredness (P<.05). Similar trends were observed for fatigue during daily activities and for the extent to which fatigue bothered subjects. Higher grip work was associated with less self-perceived fatigue on all fatigue scales (P<.01). Fatigue resistance and grip work were positively related to balance and basic mobility (all P<.01; trend for relationship between fatigue resistance and EMS). Subjects with high IL-6 and Hsp70 showed significantly worse fatigue resistance (P=.007) and muscle work (P=.045) than those with high IL-6 and low Hsp70. In male residents, higher TNF-, was related to worse fatigue resistance and grip work (P<.05). CONCLUSION: Elderly nursing home residents complaining of fatigue need to be taken seriously, because they show worse muscle endurance, which is related to poorer mobility. Inflammatory processes involving TNF-, and the interaction between IL-6 and Hsp70 are related to poorer muscle endurance in these patients. [source] Double gastric infection with Helicobacter pylori and non- Helicobacter pylori bacteria during acid-suppressive therapy: increase of pro-inflammatory cytokines and development of atrophic gastritisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2001S. Sanduleanu Background: Long-term acid suppression may accelerate the development of atrophic gastritis in Helicobacter pylori -positive subjects. The pathogenetic mechanism remains unclear. Aim: To test the hypothesis that gastric double infection with H. pylori and non -H. pylori bacterial species,during acid suppression,may result in an enhanced inflammatory response, contributing to the development of atrophic gastritis. Patients and methods: A consecutive series of patients with gastro-oesophageal reflux disease undergoing treatment with proton pump inhibitors (n=113) or histamine2 -receptor antagonists (H2 -RAs) (n=37), and 76 non-treated dyspeptic controls were investigated. Gastric mucosal H. pylori and non- H. pylori bacteria, histological gastritis, H. pylori serology, and circulating interleukin (IL)-1,, IL-6, and IL-8 were examined. Results: Patients on acid suppression with either proton pump inhibitors or H2 -RAs had a similar prevalence of H. pylori infection to the controls, but a higher prevalence of non- H. pylori bacteria (61% and 60% vs. 29%, P < 0.0001 and P < 0.002). Both the presence of H. pylori and non- H. pylori bacteria were independent risk factors of atrophic gastritis (antrum: relative risks (RRs), 10.1 and 5.07; corpus: RRs, 11.74 and 6.38). A simultaneous presence of H. pylori and non- H. pylori bacteria was associated with a markedly increased risk of atrophic gastritis (antrum: RR, 20.25; corpus: RR, 20.38), compatible with a synergistic effect. Furthermore, the simultaneous presence of both types of bacteria was associated with higher cytokine levels than in patients without any type of bacteria. This increase was also greater than in patients with H. pylori infection alone (P < 0.001, for both IL-1, and IL-8). Summary and conclusions: H. pylori -positive patients on long-term acid inhibition displayed three features: non- H. pylori bacterial growth; increased cytokine levels; and a higher risk of atrophic gastritis. We suggest that double infection with H. pylori and non- H. pyloribacteria is a major factor in the development of atrophic gastritis during gastric acid inhibition. [source] An inhibitor of interleukin-6 trans-signalling, sgp130, contributes to impaired acute phase response in human chronic liver diseaseCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2009A. Lemmers Summary In chronic liver disease, high circulating interleukin (IL)-6 contrasts with a poor acute phase response. We evaluated the impact of liver and circulating IL-6-receptor (IL-6R) forms on IL-6 bioactivity in chronic liver disease. IL-6, soluble IL-6-receptor and sgp130 levels were assayed in plasma from 45 patients with alcoholic liver disease, 84 with hepatitis C virus (HCV) infection undergoing transjugular liver biopsies and 15 healthy subjects. IL-6R mRNA was quantified on liver extracts from 54 patients with alcoholic liver disease with or without cirrhosis and 18 HCV-infected patients. The effect of gp130,Fc on fibrinogen secretion induced by IL-6 trans-signalling was evaluated on hepatocyte cultures. Levels of plasma IL-6 and sgp130, but not soluble IL-6R, increased with the stage of chronic liver disease, and correlated significantly with disease severity. Alcoholic liver disease patients had higher plasma IL-6 levels than hepatitis C, but lower liver IL-6R expression. In alcoholic and HCV-related liver diseases, liver IL-6R expression decreased with advanced fibrosis stage. In vitro, on hepatocytes, gp130,Fc blunted the acute phase response while soluble IL-6R enhanced IL-6 stimulation. In advanced chronic liver disease, high plasma IL-6 is associated with low liver IL-6R expression. This situation enables high plasma sgp130 to act as a major negative regulator of liver IL-6 trans-signalling, as demonstrated functionally here on hepatocytes. This might explain the poor acute phase response induced by IL-6 in chronic liver disease. [source] | ||||||||||