THE EFFECT OF HISTAMINE ON THE OXIDATIVE BURST OF HL-60 CELLS BEFORE AND AFTER EXPOSURE TO REACTIVE OXYGEN SPECIES

During an inflammation neutrophils are stimulated to produce reactive oxygen species (ROS). These ROS induce the release of histamine from m ast cells, which are also present at the inflammation site. In this st udy dibutyryl cAMP differentiated HL60 cells are used as a model for h uman neutrophils. The effect of histamine on formyl-methionyl-leucyl-p henylalanine (fmlp) stimulated cells is examined. Except for histamine also an accumulation of ROS takes place at the inflammation site and we investigated if ROS can influence the response of the stimulated HL 60 cells. It is found that 10(-3) M histamine can inhibit the fmlp ind uced superoxide anion radical production. This occurs partly via an H- 2 receptor because H-2 antagonists like famotidine, mifentidine and ra nitidine could partially antagonize this effect of histamine. When HL6 0 cells are exposed to hydrogen peroxide or hypochlorous acid (20 min) , an increased fmlp response is found while the inhibiting effect of h istamine remains unchanged.