Neutrophil response of transgenic mice expressing human group IIA phospholipase A2 in bacterial infections

Group IIA phospholipase A2 (PLA2) is a newly recognized acute phase protein with marked antibacterial properties. We have shown previously that transg enic C57BL/6 J mice expressing human group IIA PLA2 (PLA2(+) mice) are more resistant to bacterial infections than nontransgenic C57BL/6 J mice that, among mice, are unusual in that they lack the mouse analogue of group IIA P LA2 (PLA2(-) mice). To elucidate the possible mechanisms involved in the ho st response of these mice in bacterial infection, peripheral inflammatory c ell responses of PLA2(+) and PLA2(-) mice were studied after i.p. administr ation of Escherichia coli, E. coli lipopolysaccharide or Staphylococcus aur eus. Uninfected PLA2(+) mice had higher numbers of lymphocytes and polymorp honuclear neutrophil leukocytes (PMNs) in their blood than PLA2(-) mice. In PLA2(+) mice, the number of PMNs increased in peripheral blood in parallel with the concentration of group IIA PLA2 after the administration of bacte ria, whereas these responses were not seen in PLA2(-) mice. High concentrat ions of group IIA PLA2 in PLA2(+) mice may increase the synthesis of bioact ive molecules, such as prostaglandins, which in turn may mobilize PMNs into circulation. Our results support the hypothesis that group IIA PLA2 is an important inflammatory mediator in bacterial infections.