The Respiratory Burst of Human Granulocytes Is Mostly Independent of Potassium

Reactive oxygen species (ROS) are among the most effective tools of the innate immune response against pathogenic microbes. The respiratory burst (RB) of polymorphonuclear leukocytes (PMNs) generates an electron current that reduces molecular oxygen to superoxide. Superoxide reacts to form hydrogen peroxide as a precursor to the highly bactericidal hypochlorous acid. Here, we investigated whether alterations in extracellular potassium concentration impact H2O2 production. Such changes may occur, for example, during massive cell death due to necrosis or due to trauma injuries when potassium diffuses out of the cells. We recorded H2O2 release over a 2 h period of RB under varying potassium concentrations. Except for 100 mM potassium chloride, which increased the time delay before detectable H2O2 production, none of the potassium concentrations had a substantial effect on RB. We further examined whether this effect depended on the specific monovalent ion species. When sodium or methanesulfonate was used instead of potassium or chloride, respectively, no changes in H2O2 production were observed. Cell volume measurements under different potassium concentrations showed that only 100 mM potassium chloride significantly shrank the cells. We propose that hypertonic stress is crucial for delaying RB in human granulocytes, whereas the RB itself is independent of the tested ionic species. Additionally, the conducted hypertonic stress experiments revealed an unexpected time-dependence during the course of the RB, showing that the first 6 min were almost inert to hyperosmotic stress.