Chimerical Anti-TNF-α, Infliximab, Inhibits Neutrophil Chemotaxis and Production of Reactive Oxygen Species by Blocking the Priming Effect of Mononuclear Cells on Neutrophils

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Abstract
Clinical experience with anti-tumor necrosis factor alpha (anti-TNF-α) agents implies that these agents can cause a rapid onset amelioration of the symptoms and laboratory parameters in some inflammatory diseases. Precise explanation of this fast anti-inflammatory action is not known. The aim of our study is to investigate the direct and indirect effects of anti-TNF agents on the chemotaxis and reactive oxygen species (ROS) production of neutrophils. For this purpose, isolated neutrophil cultures (INCs) and mixed leukocyte cultures were prepared from the venous blood of healthy subjects. Those cultures were separated to different groups according to the presence of anti-TNF or the stimulation of phytohemagglutinin (PHA). In this study, anti-TNF treatment did not change the migration ability of neutrophils in INCs. However, we established that chimerical anti-TNF-α, infliximab, inhibits neutrophil chemotaxis and production of ROS by blocking the priming effect of PHA-stimulated circulating mononuclear cells. These results may explain, at least partly, the rapid onset anti-inflammatory actions of these agents observed in clinical practice.

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