SOLUBLE CD25 AND CD95 MOLECULES LEVEL AT BURNS

Cover Page


Cite item

Full Text

Abstract

Background: Burn injury is accompanied by modulation of the many components of immunity, including the system regulation, which includes soluble forms of leukocyte differentiation molecules. Earlier in burn patients, we detected changes in serum levels of soluble differentiation molecules CD25 (sCD25) and CD95 (sCD25). Despite the existence of data on change of serum level of the soluble molecules CD25 and CD95 in the blood of patients with a burn trauma, there are no data on particular cell producers.

Aims: To conduct the analysis of serum level of the molecules sCD25 and sCD95 in the blood of patients with acute burn trauma in comparison with peripheral blood cells composition to obtain data on the types of cells that produce the molecules sCD25 and sCD95.

Materials and methods: Blood samples from 24 heavily burnt patients aged 16 to 77 years were studied. Determination of sCD25 and sCD95 molecules serum levels was performed by ELISA. Number of CD45+CD25+ lymphocytes, CD45+CD95+ cells, CD14+CD95+ monocytes, CD16b+CD95+ neutrophils, and RFMI (relative mean fluorescence intensity) was evaluated by flow cytometry.

Results: In the first five days of the date of burn sCD25 and sCD95 serum levels tended to increase. sCD25 molecules contents in the blood of surviving and dead patients did not depend on the relative content of CD45+CD25+ lymphocytes, RFMI index, but correlated with the absolute level of lymphocytes and leukocytes. Serum levels of sCD95 molecules showed the dependence on the absolute neutrophil count and leukocytes in the survivors and on the absolute content of lymphocytes, neutrophils, and leukocytes in patients who died.

Conclusions: The findings suggest that the lymphocytes in the early period of burn disease are the main cells-producers of sCD25 and affect the increase of its content in the blood serum not due to changes in the density of CD25 molecules expression on their membrane followed by increased shedding but by increasing the number of CD25 positive cells. The main cells-producers of sCD95 molecules for survivors in the early period of burn disease are likely to be the neutrophils and lymphocytes; in the dead patients, the main producers are neutrophils.

Keywords

About the authors

M. Ju. Lebedev

Volga Federal Medical Research Center

Author for correspondence.
Email: miklgito@mail.ru
ORCID iD: 0000-0001-5596-2619
 

Кандидат медицинских наук, старший научный сотрудник группы иммунологии.

603155, Нижний Новгород, В. Волжская набережная, д. 18/1, тел.: +7 (951) 908-13-42.

SPIN-код: 6801-2854

Россия

M. N. Sholkina

Volga Federal Medical Research Center

Email: msholkina@inbox.ru
ORCID iD: 0000-0003-0258-3847

Кандидат медицинских наук, врач клинической лабораторной диагностики клинико-иммунологической лаборатории.

603155, Нижний Новгород, В. Волжская набережная, д. 18/1, тел.: +7 (831) 436-62-40.

SPIN-код: 9563-6356

Россия

D. V. Novikov

N.I. Lobachevskiy National Research Nizhny Novgorod State University

Email: novikov.dv75@mail.ru
ORCID iD: 0000-0001-7049-6935

Кандидат биологических наук, ведущий научный сотрудник Центра молекулярной биологии и биомедицины.

603950, Нижний Новгород, пр. Гагарина, д. 23, тел./факс: +7 (831) 419-90-64.

SPIN-код: 6801-1613

Россия

S. V. Shumilova

N.I. Lobachevskiy National Research Nizhny Novgorod State University

Email: swetlana.shumilova@gmail.com
ORCID iD: 0000-0002-2727-2888

Кандидат биологических наук, старший научный сотрудник Центра молекулярной биологии и биомедицины.

603950, Нижний Новгород, пр. Гагарина, д. 23, тел./факс: +7 (831) 419-90-64.

SPIN-код: 9562-9450

Россия

V. V. Novikov

N.I. Lobachevskiy National Research Nizhny Novgorod State University

Email: mbre@mail.ru
ORCID iD: 0000-0002-2449-7213

Доктор биологических наук, профессор, заведующий кафедрой молекулярной биологии и биомедицины.

603950, Нижний Новгород, ГСП-20, пр. Гагарина, д. 23, тел./факс: +7 (831) 462-32-16.

SPIN-код: 5492-7871

Россия

A. V. Karaulov

N.I. Lobachevskiy National Research Nizhny Novgorod State University; I.M. Sechenov Moscow State Medical University

Email: drkaraulov@mail.ru
ORCID iD: 0000-0002-1930-5424

Доктор медицинских наук, профессор, академик РАН, заведующий кафедрой клинической иммунологии и аллергологии ПМГМУ им. И.М. Сеченова

119991, Москва, ул. Трубецкая, д. 8, стр. 2, тел.: +7 (495) 635-13-73.

SPIN-код: 4122-5565

Россия

References

  1. Jewo PI, Fadeyibi IO. Progress in burns research: a review of advances in burn pathophysiology. Ann Burns Fire Disasters. 2015;28(2):105–115.
  2. Teodorczyk-Injeyan JA, McRitchie DI, Peters WJ, et al. Expression and secretion of IL-2 receptor in trauma patients. Ann Surg. 1990;212(2):202–208. doi: 10.1097/00000658-199008000-00015.
  3. Walsh DS, Siritongtaworn P, Pattanapanyasat K, et al. Lymphocyte activation after non-thermal trauma. Br J Surg. 2000;87(2):223–230. doi: 10.1046/j.1365-2168.2000.01341.x.
  4. Teodorczyk-Injeyan JA, Sparkes BG, Lalani S, et al. IL-2 regulation of soluble IL-2 receptor levels following thermal injury. Clin Exp Immunol. 1992;90(1):36–42. doi: 10.1111/j.1365-2249.1992.tb05828.x.
  5. Teodorczyk-Injeyan JA, Sparkes BG, Mills GB, Peters WJ. Immunosuppression follows systemic T lymphocyte activation in the burn patient. Clin Exp Immunol. 1991;85(3):515–518. doi: 10.1111/j.1365-2249.1991.tb05759.x.
  6. Barclay AN, Birkeland ML, Brown MH, et al, editors. The Leucocyte antigen facts book. London, UK: Academic Press; 1993. 424 p.
  7. Debatin KM, Goldmann CK, Bamford R, et al. Monoclonal-antibody-mediated apoptosis in adult T-cell leukaemia. Lancet. 1990;335(8688):497–500. doi: 10.1016/0140-6736(90)90735-N.
  8. Ricci-Vitiani L, Conticello C, Zeuner A, De Maria R. CD95/CD95L interactions and their role in autoimmunity. Apoptosis. 2000;5(5):419–424. doi: 10.1023/A:1009668212375.
  9. Hughes DP, Crispe IN. A naturally occurring soluble isoform of murine Fas generated by alternative splicing. J Exp Med. 1995;182(5):1395–1401. doi: 10.1084/jem.182.5.1395.
  10. Cascino I, Fiucci G, Papoff G, Ruberti G. Three functional soluble forms of the human apoptosis-inducing Fas molecule are produced by alternative splicing. J Immunol. 1995;154(6):2706–2713.
  11. Hosaka N, Oyaizu N, Kaplan MH, et al. Membrane and soluble forms of Fas (CD95) and Fas ligand in peripheral blood mononuclear cells and in plasma from human immunodeficiency virus-infected persons. J Infect Dis. 1998;178(4):1030–1039. doi: 10.1086/515700.
  12. Lebedev MJ, Ptitsina JS, Vilkov SA, et al. Membrane and soluble forms of Fas (CD95) in peripheral blood lymphocytes and in serum from burns patients. Burns. 2001;27(7):669–673. doi: 10.1016/S0305-4179(01)00036-5.
  13. Novikov VV, Egorova NI, Kurnikov GYu, et al. Serum levels of soluble HLA and IL-2R molecules in patients with urogenital chlamydia infection. Adv Exp Med Biol. 2007;601:285–289. doi: 10.1007/978-0-387-72005-0_30.
  14. Liles WC, Kiener PA, Ledbetter JA, et al. Differential expression of Fas (CD95) and Fas ligand on normal human phagocytes: Implications for the regulation of apoptosis in neutrophils. J Exp Med. 1996;184(2):429–440. doi: 10.1084/jem.184.2.429.
  15. Lebedev MJ, Egorova NI, Sholkina MN, et al. Serum levels of different forms of soluble CD38 antigen in burned patients. Burns. 2004;30(6):552–556. doi: 10.1016/j.burns.2004.01.029.
  16. Iwai K, Miyawaki T, Takizawa T, et al. Differential expression of Bcl-2 and susceptibility to anti-Fas-mediated cell death in peripheral blood lymphocytes, monocytes, and neutrophils. Blood. 1994;84(4):1201–1208.
  17. Kiener PA, Davis PM, Starling GC, et al. Differential induction of apoptosis by Fas-Fas ligand interactions in human monocytes and macrophages. J Exp Med. 1997;185(8):1511–1516. doi: 10.1084/jem.185.8.1511.
  18. Savill J. Apoptosis in resolution of inflammation. J Leukoc Biol. 1997;61(4):375–380.

Supplementary files

Supplementary Files
Action
1. JATS XML

Copyright (c) 2017 "Paediatrician" Publishers LLC



This website uses cookies

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

About Cookies