Tumor necrosis factor alpha and interleukin 6 productions in response to platelet-activating factor in chronic hepatitis B virus infection

WOS: 000223490600007PubMed ID: 15316260Objective: The aim of this study was to determine tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) release in response to platelet-activating factor (PAF) induction in peripheral blood mononuclear cells (PBMCs) from chronic hepatitis B virus (HBV) carriers. Methods: Subjects were grouped into three subgroups. The mean age was 37+/-10 years. Group A (n=15), group B (n=10) and group C (n=9) subjects were HBV serology-negative, had natural immunity after recovery from an acute HBV infection, and were chronic HBV carriers, respectively. Results: Compared with group A, PBMCs from naturally immune subjects and chronic HBV carriers produced significantly higher amounts of TNF-alpha and IL-6 in response to PAF. In chronic HBV carriers, TNF-alpha (1,633.3+/-793.7) and IL-6 (2,533.3+/-466.3) production was statistically lower than TNF-alpha (2,630.0+/-727.3) and IL-6 (3,870.0+/-728.4) obtained from naturally immune subjects to HBV. Conclusion: Differences of TNF-alpha levels between chronic HBV carriers and naturally immune subjects suggest that TNF-alpha may be a critical mediator of HBV clearance. Copyright (C) 2004 S. Karger AG, Basel

Does dexamethasone affect ceftriazone penetration into cerebrospinal fluid in adult bacterial meningitis

WOS: 000183033400010PubMed ID: 12727079Trough cerebrospinal fluid (CSF) ceftriaxone concentrations were measured daily to investigate the effect of dexamethasone on ceftriaxone penetration into CSF in adult patients with acute bacterial meningitis. Patients were divided into two groups in this double blind randomized study. In group 1 (n = 6) patients were given ceftriaxone with dexamethasone whereas in group 2 (n = 6) patients were only administered ceftriaxone. Plasma and CSF samples were collected at 24, 48, 72, 96 and 264 h following the study treatments. The trough CSF ceftriaxone concentrations were measured using high performance liquid chromatography (HPLC) and microbiological assay. CSF ceftriaxone concentrations were 3.21 mg/l at 24 h in group 1 and 4.85 mg/l at the same time in group 2 by HPLC. Although microbiological assay results were lower than HPLC the trough CSF ceftriaxone concentrations in dexamethasone group were at least 10(3) times higher than the minimum inhibitory concentrations of the susceptible strains. It was concluded that the ceftriaxone concentration in CSF was adequate and ceftriaxone penetration was not significantly affected by concomitant dexamethasone use in adult patients with acute bacterial meningitis. (C) 2003 Published by Elsevier Science B.V. and the International Society of Chemotherapy

The balance between the production of tumor necrosis factor-alpha and interleukin-10 determines tissue injury and lethality during intestinal ischemia and reperfusion

A major goal in the treatment of acute ischemia of a vascular territory is to restore blood flow to normal values, i.e. to "reperfuse" the ischemic vascular bed. However, reperfusion of ischemic tissues is associated with local and systemic leukocyte activation and trafficking, endothelial barrier dysfunction in postcapillary venules, enhanced production of inflammatory mediators and great lethality. This phenomenon has been referred to as "reperfusion injury" and several studies demonstrated that injury is dependent on neutrophil recruitment. Furthermore, ischemia and reperfusion injury is associated with the coordinated activation of a series of cytokines and adhesion molecules. Among the mediators of the inflammatory cascade released, TNF-alpha appears to play an essential role for the reperfusion-associated injury. On the other hand, the release of IL-10 modulates pro-inflammatory cytokine production and reperfusion-associated tissue injury. IL-1beta, PAF and bradykinin are mediators involved in ischemia and reperfusion injury by regulating the balance between TNF-alpha and IL-10 production. Strategies that enhance IL-10 and/or prevent TNF-alpha concentration may be useful as therapeutic adjuvants in the treatment of the tissue injury that follows ischemia and reperfusion