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A study of bacteremia using the baboon bacteremia model has shown that the production of tumor necrosis factor (TNF) receptors and interleukin-1 (IL-1) is under partial control of endogenous TNF. Infusion of the primates with anti-TNF attenuated the increase in soluble TNF receptors and IL-1 receptor antagonists. A similar increase was observed in the circulating levels of IL-1, IL-8, and monocyte chemotactic peptide-1.

Investigates the influence of pegylated recombinant human leptin on weight loss and inflammatory status in obese subjects. Subject characteristics; Adverse events related to treatment; Drug dosage; Drug tolerance and safety.

Lipopolysaccharide (LPS) activates both myeloid and endothelial cells. Whereas CD14 has been shown to be involved in LPS recognition by myeloid cells, the mechanism responsible for the strong response of endothelial cells to LPS remains to be elucidated. The role of CD14 in this process was studied using CD14-specific antibodies (Ab). Anti-CD14 Ab inhibited LPS-induced interleukin-6 (IL-6) release and E-selectin expression by cultured human umbilical vein endothelial cells (HUVEC). Messenger RNA encoding IL-6 and E-selectin was reduced in parallel. The inhibitory effect of anti-CD14 Ab was epitope dependent, maximal at low LPS concentrations and dropping with increasing LPS doses. Anti-CD14 Ab did not affect endothelial cell activation induced by IL-1β, tumour necrosis factor-α (TNF-α) and phorbol 12-myristate 13-acetate (PMA). IL-6 release and E-selectin expression of HUVEC were strongly reduced when LPS activation was performed in the absence of serum, indicating involvement of serum components in LPS activation of HUVEC. Nevertheless, anti-CD14 Ab also blocked LPS-induced HUVEC activation in the absence of serum. Although the role of serum components in LPS activation remains to be elucidated, CD14 seems to be a key mediator in LPS-induced activation of endothelial cells. [ABSTRACT FROM AUTHOR]

In this study we demonstrate that FcγRII on polymorphonuclear cells (PMN) (i) mediates binding of immune complexes, and (ii) is polymorphic, similar to the polymorphism described for monocytes and platelets. This was demonstrated in an adherence assay of PMN to activated human umbilical vein endothelial cells (HUVEC). Precoating of activated HUVEC with a mouse IgG1 monoclonal antibody (mAb) ENA1, which is highly reactive with activated HUVEC, caused an enhanced adhesion in 11 of 15 experiments using PMN from different donors. Enhanced adhesion of the PMN corresponded with expression of a high-responder (HR) FcγRII on monocytes isolated from the same donor, as identified by anti-CD3-induced T-cell proliferation. These data led to the conclusion that FcγRII on PMN is polyrnorphic. This conclusion was, furthermore, supported by immunofluorescence (IF) studies using a new mAb 41H16, which selectively reacts with the HR allotype of FcγRII. [ABSTRACT FROM AUTHOR]

Interleukin (IL)-6 has a limited role in the pathogenesis of the acute systemic inflammatory response syndrome elicited by bolus administration of bacteria or bacterial products. We sought to determine the role of IL-6 in septic peritonitis induced by cecal ligation and puncture (CLP). CLP led to a rapid and sustained induction of IL-6 in plasma and organ homogenates. Pretreatment (-2 h) with an anti-IL-6 mAb (1 mg) resulted in higher plasma and hepatic levels of tumor necrosis factor (TNF), as well as higher plasma concentrations of soluble TNF receptors and IL-10, while attenuating the acute phase protein response. Administration of anti-IL-6 did not influence survival. These results suggest that IL-6 production during septic peritonitis serves to inhibit the appearance of both agonist and antagonist members of the cytokine network. The importance of IL-6 in mediating the cytokine response to infection may be underestimated in more acute sepsis models. [ABSTRACT FROM PUBLISHER]

Examines the involvement of inflammatory mediators in the development of adverse reactions in filariasis patients. Association of microfilarial counts with adverse reactions; Restriction of proinflammatory responses by cytokines; Correlation between interleukin-6 and interleukin-10 concentrations.