Activity index of lymphocyte apoptosis in children with neonatal sepsis



Cite item

Full Text

Open Access Open Access
Restricted Access Access granted
Restricted Access Subscription or Fee Access

Abstract

We studied the lymphocyte apoptosis in 15 infants with late neonatal sepsis, whereas 8 of them (53.3%) were considered as a preterm infants. Etiology of sepsis was identified in 4 cases (26.7%): in 1 case of each, the cause of the disease was Klebsiella pneumoniae, Pseudomonas koreenses, Candida and St. agalactae. Control group consisted of 5 healthy newborns. Apoptosis analysis was conducted by measuring the amount of hypodiploid cells by using a propidium iodide (Sigma Aldrich) DNA staining procedure and flow cytometry (FACsCanto II, Becton Dickinson). We observed an elevated numbers of apoptotic cells in all cases of neonatal sepsis. The most significant difference was observed when the lymphocytes were cultured for 3 and 5 days. For example, on day 3 of culture the numbers of apoptotic cells in patients with neonatal sepsis vs control group were 19.6% and 5.13%, respectively. Absolute lymphopenia was noted in 26.7% of cases with neonatal sepsis. No difference in the lymphocyte apoptosis between term and preterm infants was observed. An increased amount of lymphocyte apoptosis was not associated with C-reactive protein level during the whole time-points of the experiment: at 1, 3 and 5 days. Acute phase of neonatal sepsis is associated with an increased apoptosis of peripheral blood lymphocytes.

Full Text

Restricted Access

About the authors

Kh. S Khaertynov

Kazan State Medical University

S. V Boichuk

Kazan State Medical University

V. A Anokhin

Kazan State Medical University

B. R Ramazanov

Kazan State Medical University

P. D Dunaev

Kazan State Medical University

S. F Khaiboullina

Kazan (Volga Region) Federal University

A. A Rizvanov

Kazan (Volga Region) Federal University

A. A Andreeva

Children's Republican Clinical Hospital

M. A Satrutdinov

Children's Republican Clinical Hospital

References

  1. Самсыгина Г.А. О предрасполагающих факторах и факторах риска развития неонатального сепсиса и о современных подходах его лечения. Педиатрия 2012;91(3): 32-7.
  2. Савельев В.А., Гельфанд Б.Р. Сепсис: классификация, клинико-диагностическая концепция и лечение. М.; 2013.
  3. Hotchkiss R.S., Karl I.E. The pathophysiology and treatment of sepsis. New Engl. J. Med. 2003; 348(2): 138-50.
  4. Белобородов В.Б. Иммунопатология тяжелого сепсиса и возможности ее коррекции. Вестник интенсивной терапии 2010;(4): 3-8.
  5. Hotchkiss R.S., Monneret G., Payen D. Immunosuppression in sepsis: novel understanding of the disorder and a new therapeutic approach. Lancet Infect. Dis. 2013; 13: 260-68
  6. Elmore S. Toxicologic Pathology. 2007. Vol.35, Issue: 4: 495-516
  7. Milot E., Fotouhi-Ardakani N., Filep J.G. Myeloid nuclear differentiation antigen, neutrophil apoptosis and sepsis. Front. Immunol. 2012; 3: 397.
  8. Винокуров М.Г., Юринская М.М. Регуляция апоптоза нейтрофилов при действии липополисахаридов. Биологические мембраны 2010; 27(1): 18-27.
  9. Hacker G. The morphology of apoptosis. Cell Tissue Res. 2000; 301: 5-17.
  10. Boomer J.S., To K., MD, Chang K.C. Immunosuppression in patients who die of sepsis and multiple organ failure. JAMA 2011; 306(23): 2594-605.
  11. Hotchkiss R.S., Tinsley K.W., Swanson P.E. et al. Sepsis-induced apoptosis causes progressive profound depletion of B and CD4+ T lymphocytes in humans. J. Immunol. 2001; 166: 6952-63.
  12. Hotchkiss R.S., Tinsley K.W., Swanson P.E. et al. Depletion of dendritic cells, but not macrophages, in patients with sepsis. J. Immunol. 2002; 168: 2493-500.
  13. Hotchkiss R.S., Swanson P.E., Freeman B.D. et al. Apoptotic cell death in patients with sepsis, shock, andmultiple organ dysfunction. Crit. Care Med. 1999; 27: 1230-51.
  14. Kasten K.R., Tschop J., Adediran S.G. et al. T cells are potent early mediators of the host response to sepsis. Shock 2010; 34(4): 327-36.
  15. Bochud P.Y., Calandra Th. Pathogenesis of sepsis: new concepts and implication for future treatment. BMJ 2003; 326(738): 262-5.
  16. Широкова А.В. Апоптоз. Сигнальные пути и изменение водного и ионного баланса клетки. Цитология 2007; 49(5): 385-94.
  17. Coopersmith C.M., Stromberg P.E., Dunne W.M. et al. Inhibition of intestinal epithelial apoptosis and survival in a murine model of pneumonia-induced sepsis. JAMA 2002; 287: 1716.
  18. Хаертынов Х.С., Бойчук С.В., Анохин В.А. и др. Апопотоз лимфоцитов у детей с неонатальным сепсисом. Каз. Мед. Жур. 2013; 94(5): 775-8.
  19. Riccardi C., Nicoletti I. Analysis of apoptosis by propidium iodide staining and flow cytometry. Nat. Protoc. 2006; 1(3): 1458-61.
  20. Hotchkiss R.S., Coopersmith C.M., Karl I.E. Prevention of lymphocyte apoptosis-a potential treatment of sepsis? Clin. Infect. Dis. 2005; 41: S465-9.
  21. Romagnoli C., Frezza S., Cingolani A. et al. Plasma levels of interleukin-6 and interleukin-10 in preterm neonates evaluated for sepsis. Eur. J. Pediatr. 2001; 160: 345-50.
  22. Bone R.C., Grodzin C.J., Balk R.A. Sepsis: a new hypothesis for pathogenesis of the disease process. Chest 1997; 112 (1): 235-43.
  23. Hargitai B., Szabo V., Hajdu J. et al. Apoptosis in various organs of preterm infants: histopathologic study of lung, kidney, liver, and brain of ventilated infants. Pediatr Res. 2001; 50(1): 110-4.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2014 Eco-Vector


СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: 

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies