FEATURES OF THE NEUTROPHIL GRANULOCYTE PHENOTYPE IN CHILDREN WITH INFECTIOUS MONONUCLEOSIS



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Abstract

Abstract

The nature of the course of infectious diseases caused by viruses and often their outcome is determined by the activity of the inflammatory reaction. However, the peculiarities of the neutrophil functioning during the inflammatory reaction in infectious mononucleosis (IM), caused by the Epstein-Barr virus (EBV), are currently practically not studied.

The aim of the study was to investigate the characteristics of the phenotypic composition of blood neutrophils in children with IM.

Materials and methods. 84 children aged 3 to 11 years with EBV infection of moderate severity and severe disease were examined. The control group consisted of 40 practically healthy children of a similar age range. The study of neutrophil phenotype was carried out by flow cytometry using direct immunofluorescence of whole peripheral blood.

Results. It was found that in children with MI, regardless of age, the main fraction of blood neutrophils are CD64-CD32--cells whereas in healthy children – CD64-CD32+ neutrophils. The main fraction of neutrophils in the paired combination of CD64 and CD11b antigens in sick children aged 3–6 and 7–11 years is determined to be the same as in healthy ones (CD64-CD11b+), but with a change in the content of minor cell fractions. The number of CD64-CD15+ neutrophils (the main fraction of cells in healthy children) in patients of both age groups is significantly reduced. However, there is a marked increase in the level of double-negative cells for the CD64 and CD15 antigens. At the same time, the content of double-negative neutrophils according to these markers also increases in sick children of both age groups. Cells with the CD11b-CD15+ and CD11b+CD15+ phenotypes are the main fractions in IM based on the paired combination of CD11b and CD15 antigens; in healthy children - only CD11b+CD15+ neutrophils.

Conclusion. Changes in the phenotype of neutrophils during IM characterize a decrease in the migration ability of cells with high activity of proinflammatory functions. The ontogenetic features of the neutrophil phenotype have been established which change significantly in children with IM that is apparently determined by the immunopathogenesis of the viral infection.

About the authors

Andrei Anatyevich Savchenko

Federal Research Center «Krasnoyarsk Science Center» of the Siberian Branch of the Russian Academy of Sciences, Scientific Research Institute of medical problems of the North, Krasnoyarsk, Russia

Email: aasavchenko@yandex.ru

MD, professor, head of a laboratory; Federal Research Center «Krasnoyarsk Science Center» of the Siberian Branch of the Russian Academy of Sciences, Scientific Research Institute of medical problems of the North

Russian Federation

Galina Petrovna Martynova

FSBEI of Higher Education «Prof. V.F. Voino-Yasenetsky Krasnoyarsk State Medical University» of the Ministry of Healthcare of the Russian Federation, Krasnoyarsk, Russia

Email: doc-martynova@yandex.ru

MD, professor, head of a department

Russian Federation

Lyubov Alexandrovna Ikkes

FSBEI of Higher Education «Prof. V.F. Voino-Yasenetsky Krasnoyarsk State Medical University» of the Ministry of Healthcare of the Russian Federation, Krasnoyarsk, Russia

Email: likkes@bk.ru

assistant of a department

Russian Federation

Vasilij Dmitrievich Belenjuk

Federal Research Center «Krasnoyarsk Science Center» of the Siberian Branch of the Russian Academy of Sciences, Scientific Research Institute of medical problems of the North, Krasnoyarsk, Russia

Email: dyh.88@mail.ru

Jr. researcher of a laboratory

Russian Federation

Alexandr Gennadyevich Borisov

Federal Research Center «Krasnoyarsk Science Center» of the Siberian Branch of the Russian Academy of Sciences, Scientific Research Institute of medical problems of the North, Krasnoyarsk, Russia

Author for correspondence.
Email: 2410454@mail.ru

PhD, leading researcher of a laboratory

Russian Federation

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Copyright (c) Savchenko A., Martynova G.P., Ikkes L.A., Belenjuk V.D., Borisov A.G.

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