Abstract
The production of reactive oxygen species (ROS) by polymorphonuclear leukocytes (PMN) can be induced by immune complexes and is an important component of phagocytosis in the killing of microorganisms, but can also be involved in inflammatory reactions when immune complexes are deposited in tissues. We have observed that fluid-phase IgG can inhibit the generation of ROS by rabbit PMN stimulated with precipitated immune complexes of IgG (ICIgG) in a dose-dependent manner, acting as a modulatory factor in the range of physiological IgG concentrations. This inhibitory effect is compatible with the known affinity (Kd) of monomeric IgG for the receptors involved (FcRII and FcRIII). The presence of complement components in the immune complexes results in a higher stimulation of ROS production. In this case, however, there is no inhibition by fluid-phase IgG. The effect of complement is strongly dependent on the presence of divalent cations (Ca2+ or Mg2+) in the medium, whereas the stimulation of ICIgG (without complement) does not depend on these cations. We have obtained some evidence indicating that iC3b should be the component involved in the effect of complement through interaction with the CR3 receptor. The absence of the inhibitory effect of fluid-phase IgG in ROS production when complement is present in the immune complex shows that complement may be important in vivo not only in the production of chemotactic factors for PMN, but also in the next phase of the process, i.e., the generation of ROS.
Highlights
It is well known that polymorphonuclear leukocytes (PMN) can undergo a rapid metabolic change, known as the respiratory burst, when exposed to a variety of stimuli [1]; this includes an increased rate of oxygen consumption, a marked activation of the pentose-phosphate pathway and the generation of reactive oxygen species (ROS; O2, H2O2, OH·, singlet oxygen, etc.)
It is well established that the interaction of particles or surfaces with leukocytes mediated by Fcγ receptors can trigger the respiratory burst
Some experiments have shown that C3b or iC3b is not able to induce the generation of ROS by human monocytes and PMN [3]; other observations, have indicated an active role of these complement components in triggering the respiratory burst [4,5]
Summary
It is well known that polymorphonuclear leukocytes (PMN) can undergo a rapid metabolic change, known as the respiratory burst, when exposed to a variety of stimuli [1]; this includes an increased rate of oxygen consumption, a marked activation of the pentose-phosphate pathway and the generation of reactive oxygen species (ROS; O2-, H2O2, OH·, singlet oxygen, etc.). The production of these highly reactive compounds which have microbicidal properties is a component of the process of phagocytosis, being implicated in the mechanisms of defense. Some evidence has been presented indicating that the production of ROS by PMN is dependent on a synergic mechanism involving Fcγ and complement receptors [6]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
