Proinflammatory cytokine inhibitors, TNF-alpha and oxidative burst of polymorphonuclear leukocytes in the pathogenesis of sepsis in newborns.

A bstract. T his study was to evaluate the levels of the proinflammatory cytokine tumor necrosis factor α (TNF-α) a nd the cytokine inhibitors soluble TNF-α receptor (sTNFR) and interleukin (IL-1) receptor antagonist (IL-1ra), as well as the intensity of oxidative metabolism of peripheral blood polymorphonuclear leukocytes in the course of sepsis in newborns. An increase of TNF-α, sTNFR and IL-1ra concentrations was found in the blood serum o f the patients at the time of diagnosis. This was further accompanied by polymorphonuclear leukocyte stimulation and, as a consequence of prolonged bacterial antigen stimulation, functional exhaustion of these cells and their d iminished oxidative metabolism was observed. Within the same time period, an enhanced expression of p55 and p75 TNF-α receptors on polymorphonuclear leukocyte cell surfaces was found. It was indicated that t he applied p harmacotherapy caused a decrease of the initially elevated concentrations of TNF-α and proinflammatory cytokine inhibitors (sTNFR, IL-1ra). The intensive therapy of sepsis was associated with the increased oxidative burst of polymorphonuclear leukocytes along with the decrease of p55 and p75 expression on their cell surfaces.