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Biomedical subjects

K Close

Publications and source records attributed to K Close.

6 recordsLinked to original sources
PubMed1993

Morphine inhibits the release of tumor necrosis factor in human peripheral blood mononuclear cell cultures.

Opiates modulate a variety of immune responses of peripheral blood mononuclear cells (PBMC). When PBMC were treated with morphine for 24 h, cells released less (P < 0.05) bioactive TNF, a cytokine important in host defense, in the following 24-h incubation period when stimulated with lipopolysaccharide and phytohemagglutinin. Morphine alone did not significantly alter the release of TNF from PBMC cultures. Pretreatment of PBMC cultures for 1 h with naloxone blocked (P < 0.05) the inhibitory effect of morphine on the release of TNF upon stimulation with phytohemagglutinin, but not with lipopolysaccharide, suggesting the involvement of an opioid receptor. The mechanism of morphine-induced suppression of TNF release appears to be counteracted by the effect of this opiate on the release of transforming growth factor (TGF)-beta, since antibodies to this immunoregulatory cytokine further enhanced morphine-related inhibition of TNF release. Taken together, these findings indicate that morphine suppresses the release of bioactive TNF from PBMC and that TGF-beta plays a modulatory role in this inhibitory process.

Adult↗
PubMed1992

Immunologically mediated fatigue: a murine model.

Chronic fatigue syndrome (CFS) is an idiopathic disorder in which the chief symptoms is profound fatigue. To explore the relationship between immune stimulation and fatigue, we developed a murine model for quantifying fatigue: reduction in voluntary running and delayed initiation of grooming after swimming. Inoculation of female BALB/c mice with Corynebacterium parvum antigen or the relatively avirulent Me49 strain of Toxoplasma gondii induced fatigue: baseline running reduced to less than 50 and 30% for 8 and 14 days, respectively, and delayed initiation of grooming after swimming in both immunologically stimulated groups. A threefold evaluation of serum transforming growth factor-beta levels, a cytokine increased in CFS patients, was found in fatigued C. parvum- and T. gondii-inoculated mice. This murine model appears promising for investigation of the pathogenesis of immunologically mediated fatigue.

Animals↗
PubMed1992

Cytokine release from microglia: differential inhibition by pentoxifylline and dexamethasone.

Cytokines have been implicated in the pathogenesis of gram-negative bacterial meningitis. The effects of pentoxifylline and dexamethasone on the release of tumor necrosis factor (TNF), interleukin (IL)-1, and IL-6 from primary murine microglial cell cultures were explored using bioassays. When added concomitantly with lipopolysaccharide, pentoxifylline blocked the release of TNF and IL-1 but not IL-6, while dexamethasone inhibited the release of TNF and IL-6. After a 2-h exposure of microglia to lipopolysaccharide, pentoxifylline but not dexamethasone still inhibited the release of TNF. Release of TNF was enhanced 20-fold by priming of the microglia with interferon-gamma; only pentoxifylline blocked the priming effect of interferon-gamma on TNF release. These results demonstrate that pentoxifylline and dexamethasone differentially regulate the release of cytokines in microglial cell cultures and provide potential insight into their role in the treatment of gram-negative bacterial meningitis.

Animals↗