CORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 2

Traumatic brain injury (TBI) commonly proceeds as a severe disease with high morbidity that can lead to neurological disorders in some of these patients. TBI is associated by multidirectional abnormalities of immune system, which affect quantity and functions of T-, B-, and NK-lymphocytes leading to...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: S. N. Shanin, E. E. Fomicheva, T. A. Filatenkova, N. B. Serebryanaya
Formato: article
Lenguaje:RU
Publicado: SPb RAACI 2018
Materias:
Acceso en línea:https://doaj.org/article/0be72a41f2e4485d9fffca231a76809a
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:0be72a41f2e4485d9fffca231a76809a
record_format dspace
spelling oai:doaj.org-article:0be72a41f2e4485d9fffca231a76809a2021-11-18T08:03:47ZCORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 21563-06252313-741X10.15789/1563-0625-2018-2-171-178https://doaj.org/article/0be72a41f2e4485d9fffca231a76809a2018-03-01T00:00:00Zhttps://www.mimmun.ru/mimmun/article/view/1488https://doaj.org/toc/1563-0625https://doaj.org/toc/2313-741XTraumatic brain injury (TBI) commonly proceeds as a severe disease with high morbidity that can lead to neurological disorders in some of these patients. TBI is associated by multidirectional abnormalities of immune system, which affect quantity and functions of T-, B-, and NK-lymphocytes leading to infectious complications or autosensibilization. Restoration of the disturbances in neuroimmune interactions after TBI may be achieved by means of immunomodulators that have neuroprotective properties and may potentially initiate regenerative CNS activity. IL-2 is a cytokine that possesses neurooperative and neuroprotective properties. In immune system, IL-2 is produced by T-cells in response to antigen stimuli; in CNS, by brain cells. Lack of IL-2 production by both T-lymphocytes and brain cells increases a possibility of autoimmune and inflammatory pathologies. The objective of present study was to evaluate possible effects of human recombinant IL-2 (rIL-2, Roncoleukin®, Biothech Ltd., Russia) upon state and correction of immune and neuro-endocrine TBI consequences. The study was performed in adult Wistar rats. Mechanical TBI was produced by the dropping load model. 72 hours after inflicting the TBI, r-IL-2, at dose 30 mg/kg was injected once a day for three times. The animals from control group received 0.15M NaCl solution over the same period. The results have shown that, within first hours and days after TBI, corticosterone levels showed a sharp increase, whereas testosterone concentrations were decreased.In parallel, an increase in cytotoxic and proliferative activity of splenocytes was revealed, as well as increased number of splenocytes at their late apoptotic stage. Three daily injections of rIL-2 resulted into a significant increase in corticosterone and testosterone levels in injured animals on the day 7 after TBI. The animals treated with rIL-2 have exhibited more rapid normalization of cytotoxic and proliferative activity of splenocytes and return to normal ratio of proliferating splenocytes vs. apoptotic cells. Therefore, usage of rIL-2 may correct neuro-endocrine and immune interaction disturbances after TBI and decrease risk of chronic neurological disorders in TBI patients.S. N. ShaninE. E. FomichevaT. A. FilatenkovaN. B. SerebryanayaSPb RAACIarticletraumatic brain injuryexperimentalril-2corticosteronetestosteronecytotoxicitylymphocyte proliferationapoptosisImmunologic diseases. AllergyRC581-607RUMedicinskaâ Immunologiâ, Vol 20, Iss 2, Pp 171-178 (2018)
institution DOAJ
collection DOAJ
language RU
topic traumatic brain injury
experimental
ril-2
corticosterone
testosterone
cytotoxicity
lymphocyte proliferation
apoptosis
Immunologic diseases. Allergy
RC581-607
spellingShingle traumatic brain injury
experimental
ril-2
corticosterone
testosterone
cytotoxicity
lymphocyte proliferation
apoptosis
Immunologic diseases. Allergy
RC581-607
S. N. Shanin
E. E. Fomicheva
T. A. Filatenkova
N. B. Serebryanaya
CORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 2
description Traumatic brain injury (TBI) commonly proceeds as a severe disease with high morbidity that can lead to neurological disorders in some of these patients. TBI is associated by multidirectional abnormalities of immune system, which affect quantity and functions of T-, B-, and NK-lymphocytes leading to infectious complications or autosensibilization. Restoration of the disturbances in neuroimmune interactions after TBI may be achieved by means of immunomodulators that have neuroprotective properties and may potentially initiate regenerative CNS activity. IL-2 is a cytokine that possesses neurooperative and neuroprotective properties. In immune system, IL-2 is produced by T-cells in response to antigen stimuli; in CNS, by brain cells. Lack of IL-2 production by both T-lymphocytes and brain cells increases a possibility of autoimmune and inflammatory pathologies. The objective of present study was to evaluate possible effects of human recombinant IL-2 (rIL-2, Roncoleukin®, Biothech Ltd., Russia) upon state and correction of immune and neuro-endocrine TBI consequences. The study was performed in adult Wistar rats. Mechanical TBI was produced by the dropping load model. 72 hours after inflicting the TBI, r-IL-2, at dose 30 mg/kg was injected once a day for three times. The animals from control group received 0.15M NaCl solution over the same period. The results have shown that, within first hours and days after TBI, corticosterone levels showed a sharp increase, whereas testosterone concentrations were decreased.In parallel, an increase in cytotoxic and proliferative activity of splenocytes was revealed, as well as increased number of splenocytes at their late apoptotic stage. Three daily injections of rIL-2 resulted into a significant increase in corticosterone and testosterone levels in injured animals on the day 7 after TBI. The animals treated with rIL-2 have exhibited more rapid normalization of cytotoxic and proliferative activity of splenocytes and return to normal ratio of proliferating splenocytes vs. apoptotic cells. Therefore, usage of rIL-2 may correct neuro-endocrine and immune interaction disturbances after TBI and decrease risk of chronic neurological disorders in TBI patients.
format article
author S. N. Shanin
E. E. Fomicheva
T. A. Filatenkova
N. B. Serebryanaya
author_facet S. N. Shanin
E. E. Fomicheva
T. A. Filatenkova
N. B. Serebryanaya
author_sort S. N. Shanin
title CORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 2
title_short CORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 2
title_full CORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 2
title_fullStr CORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 2
title_full_unstemmed CORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 2
title_sort correction of disturbed neuroimmune interactions in experimental traumatic brain injury by means of recombinant interleukin 2
publisher SPb RAACI
publishDate 2018
url https://doaj.org/article/0be72a41f2e4485d9fffca231a76809a
work_keys_str_mv AT snshanin correctionofdisturbedneuroimmuneinteractionsinexperimentaltraumaticbraininjurybymeansofrecombinantinterleukin2
AT eefomicheva correctionofdisturbedneuroimmuneinteractionsinexperimentaltraumaticbraininjurybymeansofrecombinantinterleukin2
AT tafilatenkova correctionofdisturbedneuroimmuneinteractionsinexperimentaltraumaticbraininjurybymeansofrecombinantinterleukin2
AT nbserebryanaya correctionofdisturbedneuroimmuneinteractionsinexperimentaltraumaticbraininjurybymeansofrecombinantinterleukin2
_version_ 1718422333029351424