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...

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Main Authors: S. N. Shanin, E. E. Fomicheva, T. A. Filatenkova, N. B. Serebryanaya
Format: Article
Language:Russian
Published: St. Petersburg branch of the Russian Association of Allergologists and Clinical Immunologists 2018-03-01
Series:Медицинская иммунология
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Online Access:https://www.mimmun.ru/mimmun/article/view/1488
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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
collection DOAJ
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.
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spelling doaj-art-0be72a41f2e4485d9fffca231a76809a2025-08-20T03:37:44ZrusSt. Petersburg branch of the Russian Association of Allergologists and Clinical ImmunologistsМедицинская иммунология1563-06252313-741X2018-03-0120217117810.15789/1563-0625-2018-2-171-1781004CORRECTION OF DISTURBED NEUROIMMUNE INTERACTIONS IN EXPERIMENTAL TRAUMATIC BRAIN INJURY BY MEANS OF RECOMBINANT INTERLEUKIN 2S. N. Shanin0E. E. Fomicheva1T. A. Filatenkova2N. B. Serebryanaya3Institute of Experimental MedicineInstitute of Experimental MedicineInstitute of Experimental MedicineInstitute of Experimental Medicine; St. Petersburg State University; I. Mechnikov North-Western State Medical UniversityTraumatic 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.https://www.mimmun.ru/mimmun/article/view/1488traumatic brain injuryexperimentalril-2corticosteronetestosteronecytotoxicitylymphocyte proliferationapoptosis
spellingShingle 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
Медицинская иммунология
traumatic brain injury
experimental
ril-2
corticosterone
testosterone
cytotoxicity
lymphocyte proliferation
apoptosis
title 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_short 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
topic traumatic brain injury
experimental
ril-2
corticosterone
testosterone
cytotoxicity
lymphocyte proliferation
apoptosis
url https://www.mimmun.ru/mimmun/article/view/1488
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