We determined the degree of activation of the TNF alpha system and the levels of IL-8 in HIV-1 infection. TNF alpha is one of the most potent agents for the induction of IL-8. TNF alpha may be cleared rapidly from the circulation, however soluble tumor necrosis factor receptor (sTNFR) p75 which is more stable may reflect the degree of activation of the TNF alpha system. We measured concentrations of sTNFR p75 and IL-8 with immunoassays in the plasma of 99 HIV-1-infected patients at different stages of disease (Centers for Disease Control classification) and in 20 healthy control subjects. Plasma levels of sTNFR p75 were elevated in most of the asymptomatic seropositive patients without CD4+ T cell depletion (Stage IIA) and in most of patients of all clinical groups compared with controls. However, in the majority of those patients plasma levels of IL-8 were not higher than those of controls. Our results suggest that sTNFR p75 levels but not IL-8 levels in circulating blood are high in the course of HIV-1 infection.
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http://dx.doi.org/10.1016/0165-2478(96)02583-7 | DOI Listing |
Psychiatr Danub
September 2016
Department of Psychological Medicine, King's College London, 103 Denmark Hill, London SE5 8AF, UK,
Background: Changes in serum concentrations of tumor necrosis factor-α (TNF-α) and its soluble receptors (sTNF-R) p55 and p75 have been shown to be associated with various psychiatric treatments.
Subjects And Methods: Before and after treatment, serum levels of TNF-α, sTNF-R p55 and sTNF-R p75 were measured in 38 German soldiers who had been deployed abroad and suffered from combat-related post-traumatic stress disorder (PTSD). Patients were randomized either to inpatient psychotherapy (N=21) including eye movement desensitization and reprocessing (EMDR) or to outpatient clinical management (N=17).
Eur Cytokine Netw
September 2015
Department of Psychiatry, Psychotherapy and Psychotraumatology, Bundeswehr Hospital, Berlin, Germany.
Growing evidence suggests involvement of the tumor necrosis factor (TNF)-α system in the pathophysiology of psychiatric disorders. Research into post-traumatic stress disorder (PTSD) has investigated serum levels of TNF-α, but not to date its soluble receptors sTNF-R p55 and sTNF-R p75. We examined serum levels of TNF-α, sTNF-R p55 and sTNF-R p75 in 135 male German soldiers 70 of whom had been deployed abroad and 65 in Germany only.
View Article and Find Full Text PDFJ Nutr
February 2016
Institute of Clinical Chemistry, University of Zurich, Zurich Switzerland; and.
Background: Trimethylamine-N-oxide (TMAO) is a metabolite of carnitine, choline, and phosphatidylcholine, which is inversely associated with survival of cardiovascular disease (CVD) patients.
Objective: We examined the associations of diet with plasma concentrations of TMAO, choline, and betaine and the associations of TMAO with plasma concentrations of various cytokines.
Methods: Plasma TMAO, choline, and betaine concentrations were measured using LC-high resolution mass spectrometry in 271 participants, ≥18 y old, of the Second Bavarian Food Consumption Survey, conducted in 2002 and 2003.
Transl Res
July 2012
Department of Physiology, University of Kentucky Medical Center, Lexington, KY, USA.
Many aspects of tissue damage after acute or chronic inflammatory reactions can be attributed directly to the concomitant biosynthesis and release of inducible early proinflammatory cytokine tumor necrosis factor alpha (TNFα). Conversely, systemic inflammation is impacted by the consequences of tissue damage. Dysregulated TNFα contributes to numerous pathophysiologic conditions including inflammatory bowel disease (IBD) and arthritis.
View Article and Find Full Text PDFJ Appl Physiol (1985)
July 2011
Section of Anaesthetics, Pain Medicine, and Intensive Care, Imperial College London, Chelsea and Westminster Hospital, 369 Fulham Rd., London SW10 9NH, UK.
Elevated soluble tumor necrosis factor-α receptor (sTNFR) levels in bronchoalveolar lavage fluid (BALF) are associated with poor patient outcome in acute lung injury (ALI). The mechanisms underlying these increases are unknown, but it is possible that pulmonary inflammation and increased alveolar epithelial permeability may individually contribute. We investigated mechanisms of elevated BALF sTNFRs in two in vivo mouse models of ALI.
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