Peculiarities of leukocyte apoptosis modulation in children with pyelonephritis

One of the leading places among inflammatory diseases of the urinary tract of children belongs to pyelonephritis, the course of which presents in most cases as a severe infectious disease threatening the patient’s life, which is the main reason for development of chronic kidney failure. This study was conducted to compare apoptosis stages in peripheral blood of children of different age categories with pyelonephritis depending on etiological factor and complications. The problem of mechanisms underlying immune system misregulation, especially functional activity of leukocytes in children with pyelonephritis, have not been explored in recent years. Assessment of leukocytes (neutrophils) apoptosis stages in peripheral blood of children of different age categories with pyelonephritis depending on complications and etiological factor was the aim of present study. The children's peripheral blood samples were analysed and assessed using a flow cytofluorimeter. The present study demonstrates an increase of the level of apoptotic cells at an early stage of apoptosis in children of all age categories with chronic pyelonephritis, which can be explained by associations of a wide range of pathogens and the presence of sequelae. An increase in the number of apoptotic cells in the late stage of apoptosis is observed in children aged 1 month – 8 years, in children 8–18 years, the amount of apoptotic cells is reduced by 1.5 times. The study of apoptosis stages allows complete characterization of the dynamics of the apoptotic process and supplementation of the pathogenesis of pyelonephritis in children. Such studies will make it possible to affect apoptosis modulation to regulate or correct it and encourage the finding of innovative solutions in the treatment related to influence on the immune response. We conclude that enhancement of peripheral blood leukocyte apoptosis in chronic form of pyelonephritis especially in young children is due to the polyetiology of this form of pyelonephritis and the development of complications.

Autoimmune Lymphoproliferative Syndrome (ALPS): A Case Report

Background: Autoimmune lymphoproliferative syndrome (ALPS) is a rare disorder of the blood, estimated at around 500 cases worldwide. It is characterized by a dysregulation of T-cells in the immune system, and is caused by a defect in the process that mediates leukocyte apoptosis. This may result in an increased risk of lymphoma and autoimmune diseases. Case: The author reports a case of an 11-year-old male who had been followed up since three years of age for recurrent cytopenias, occurring with intermittent breakouts of purpuric rash, nosebleeds, and prolonged infections. Conclusion: A probable diagnosis was made through criteria based on the First International ALPS workshop of 2009. This includes the presence of circulating double-negative T cells, considered the laboratory marker unique for ALPS. The mainstay of treatment was prednisone, given at doses varying in proportion to the severity of immunocytopenia. osis.

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

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.