The effect of acute phase proteins on the activity of peripheral blood neutrophils

Abstract

Neutrophils are the leading cells of the innate immune system and the main population of leukocytes responsible for the primary reaction of the organism to various infectious agents. The latter are destroyed by neutrophils during the processes of phagocytosis and a cascade of reactions, including the respiratory burst. As a result of the respiratory burst, neutrophils produce reactive oxygen and halogen species, which are powerful cytotoxic agents which destroy foreign particles in the phagolysosome. All of these processes require strict regulation, since excessive activation of neutrophils may lead to higher production of reactive oxygen species thereby causing tissue damage in the focus of inflammation. Acute phase proteins may play a role as regulators of inflammatory processes. Our previous works have shown that ceruloplasmin is involved in the inhibition of the respiratory burst of neutrophils in whole blood samples. Fibrinogen, on the contrary, increased the intensity of respiratory burst. A detailed characterization of the effects acute phase proteins exert on peripheral blood neutrophils’ functions has been studied not for all acute phase proteins and especially their combinations. In this paper, for the first time, the flow cytometer and registration of reactive oxygen species production in peripheral blood cells have been used to study the effects of several acute phase reactants (C-reactive protein, serum amyloid A, alpha-1-acid glycoprotein and fibrinogen) on the ability of peripheral blood neutrophils to activate respiratory burst. The results showed that significant changes in the capacity of reactive oxygen species production by neutrophils were seen for a set of combinations of the studied acute phase proteins. The study of the interaction of ceruloplasmin and fibrinogen with peripheral blood neutrophils revealed that they were localized to the membrane. It seems promising to identify receptors for acute phase proteins at the neutrophil membrane.