ABSTRACT
Inappropriate induction of neutrophil apoptosis during infection could deplete neutrophil numbers and function, impairing host defense and favoring bacterial persistence. The aim of this work was to determine whether infection could promote neutrophil apoptosis by evaluating the rate of neutrophil apoptosis in sera of patients with pneumonia and healthy control patients. It also aimed at examining the role of FasL in infection induced neutrophil apoptosis. This study included 25 patients diagnosed as having pneumonia and 15 healthy controls. Neutrophil apoptosis was quantified by flow cytometry using propidium iodide and Becton Dickinson FACScalibur. The rate of apoptosis was greater for neutrophils isolated from patients with pneumonia than for healthy controls [P value, 0.000]. Patients with gram negative and severe infections exerted a higher rate of neutrophil apoptosis than patients with gram positive infection. The rate of neutrophil apoptosis was greater when subjected to sera from patients with either gram-negative or gram-positive infection than when subjected to sera from controls [P value, 0.001]. Moreover, anti-FasL antibody-neutralized infected sera attenuated the infected-serum-induced neutrophil apoptosis [P value, 0.000]. These results suggest that infection enhances neutrophil apoptosis possibly through FasL but its source needs to be determined in further studies