Fig. 1

Activation of neutrophil granulocytes and the kallikrein-kinin system. During neutrophil activation triggered by different substances, the released neutrophil elastase could cleave and inactivate C1-INH [12]. Besides, activated neutrophils can release neutrophil extracellular traps, and both processes may contribute to bradykinin release [13, 15]. On the other hand, high molecular weight kininogen and factor XII can attach directly to the surface of NGs. Prekallikrein, by contrast, binds to the cell membrane indirectly, through its docking protein, high molecular weight kininogen, which could create the conditions for the release of kinins (bradykinin and kallidin) through the activation of the cell-bound kallikrein-kinin system. This would be manifested by the factor XII-mediated activation of prekallikrein on one hand, and/or by the release of neutrophil-borne, active tissue kallikrein on the other [17]. [Abbreviations: IL = interleukin, TNF-α = tumor necrosis factor-α, LPS = lipopolysacharide, HK = high molecular weight kininogen, PK = prekallikrein, tKal = tissue kallikrein, LK = low molecular weight kininogen, C1-INH = C1-inhibitor, FXII = factor XII, MPO = myeloperoxidase, PTX3 = pentraxin 3]