Aim: 

Neutrophils belong to the first cell population infiltrating into the inflammation site. It is well known that the defence mechanisms of these cells include efficient radical production which during the defence response can at the same time damage the host tissue causing e.g. lipid peroxidation. Therefore, it is important to know how the cells are activated in different pathophysiological conditions.

Methods: 

Subjects were febrile infectious patients having either microbiologically confirmed or clinically diagnosed bacterial or viral infection, and healthy controls. Receptor expression of Fcg-receptors I, II, and III, as well as complement receptors CR1 and CR3 were determined using fluoresecence-labeled receptor-specific monoclonal antibodies and flow-cytometry. Radical production was determined luminometrically by measuring luminol-amplified chemiluminescence emission from neutrophils stimulated with opsonized or nonopsonized zymosan.

Results: 

The phenotype of neutrophils of infectious patients differs from that of healthy controls. In viral infections FcgRI expression is markedly increased while CR3 expression is only slightly increased compared to controls. On the other hand, in bacterial infections the expression of CR1, CR3 and FcgRI is much higher than in healthy controls. Radical production in whole blood samples (ex vivo conditions) stimulated with opsonized zymosan is proportional to the number of neutrophils in the sample. However, when the cells from bacterial infection patients are stimulated with nonopsonized zymosan, radical production is about double compared to that of viral infection patients or healthy controls.

Conclusion: 

The increased expression of complement receptors on neutrophils reflects the increased activity of neutrophils to produce reactive oxygen species. Which part of this increased production is intracellular and which part is released extracellularly remains to be elucidated