Polymorphonuclear Leukocyte Apoptosis Is Accelerated by Sulfatides or Sulfatides-TreatedSalmonellaTyphimurium Bacteria

Abstract

Neutrophils die by apoptosis following activation and uptake of microbes or enter apoptosis spontaneously at the end of their lifespan if they do not encounter a pathogen. Here we report that sulfatides or sulfatides-treatedSalmonellaTyphimurium bacteria accelerated human neutrophil apoptosis. Neutrophil apoptosis was examined by flow cytometry. Sulfatides caused prominent increase in percentage of apoptotic cells after 2.5 hrs of incubation.SalmonellaTyphimurium bacteria by themselves did not affect the basal level of apoptosis in neutrophil population. When neutrophils were added toS.Typhimurium “opsonized” by sulfatides, apoptotic index significantly increased, whereas the number of phagocyting cells was not influenced. Sulfatides’ proapoptotic effect was strongly dependent on the activity ofβ-galactosidase; inhibition of this enzyme impaired its potency to accelerate apoptosis. These data support the mechanism of neutrophil apoptosis triggering based on sulfatides’ ability to accumulate in intracellular compartments and mediate successive increase in ceramide content resulting fromβ-galactosidase activity.