Gastritis is characterized by a massive accumulation of polymorphonuclear neutrophils in the gastric mucosa. Although the oxidative burst is activated, no phagocytic killing takes place when unopsonised Helicobacter pylori is phagocytosed by neutrophils. The free oxygen radicals that are produced may instead leak out of the cell and cause damage to the surrounding tissue. This type of tissue damage has been associated with gastric ulcers and gastric cancer. The importance of a close control of this effector function is evident. Through the methods of immune blotting and flow cytometry, and by means of the known inhibitors wortmannin, PD98059 and SB203580, the possible involvement of three protein kinases with the Helicobacter pylori induced oxidative burst was studied. The protein kinases which were studied are extracellular regulated protein kinase (ERK), p38 MAPK and phosphatidyl inositol-3-kinase (PI3K). According to the results that were received, the neutrophil oxidative burst induced by Helicobacter pylori is activated via a signal transduction pathway mediated by PI3K, where ERK is involved either downstream of PI3K, or on a pathway parallel but necessary to the PI3K mediated pathway. The third protein kinase that was studied, p38 MAPK, seems to bee involved to a lesser extent in the activation of the Helicobacter pylori induced oxidative burst in neutrophils. Keywords: Mitogen activated protein kinase, phosphatidyl inositol-3-kinase, oxidative burst, flow cytometry, immune blotting.