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DYNAMICS OF CHANGES IN THE IMMUNOLOGICAL STATUS INDUCED BURNDICALLY DISEASES
Radjapov Adilbek Anvarbekovich, Urgench Branch of the Tashkent Medical Academy E-mael: mbshakur@mail.ru
DYNAMICS OF CHANGES IN THE IMMUNOLOGICAL STATUS INDUCED BURNDICALLY DISEASES
Abstract: It was found that in rats with an induced burn disease, significant immune status disorders were detected, which were determined by quantitative T-cell and neutrophilic immunodeficiency with an increase in natural killers and activation of the apoptosis process.
Keywords: burn disease in experiment, immunological status.
According to the World Health Organization, thermal injuries rank third among other injuries, accounting for 10-11%. In terms of the duration and severity of the course, burn disease is in the lead among various variants of traumatic illness. Burn disease should be considered as an immunodeficiency disease, in which there is an early and prolonged decline in the rates of congenital and acquired immunity [2; 6]. It should be borne in mind that the immune response of heavy burns develops against the backdrop of the acute shortage of energy and plastic resources [3; 4]. The immune status of patients with severe thermal trauma is ultimately formed against the backdrop of a large number of immunosuppressive factors: extensive skin damage as an immune organ, stress during trauma, exposure to a large number of toxins of fired tissues, increased lipid peroxidation and disruption of the membrane cell systems, antibiotic therapy, hormone therapy, multiple anesthesia during dressings and operations of autodermoplasty [1; 3]. In severe thermal damage, cellular defense mechanisms are particularly inhibited. Significant inhibition of T- and B-systems of immunity leads to a sharp decrease in the body's resistance to infectious agents, which can become a prerequisite for the development of both local and general infectious complications, up to burn sepsis [5].
However, to date, there is a small number of works devoted to a comprehensive study of the immunological status of burned and the role of their disorders in the pathogenesis of burn disease and its complications.
The purpose of the study: to study changes in the indices of the immune status in the dynamics of the development of burn disease in the experiment
Materials and methods: a deep thermal skin burn (IIIB degree) was induced on 54 non-native white rats in females weighing 140-270 g. Under ether anesthesia, a burn in animals was caused by applying a metal plate heated to 1000 C to the skin of the back. Exposure time of the plate, the area of 18-20% of the total surface of the skin of the rat, through a wet napkin was 16 seconds. With these exposure modes, damage to all layers of the skin was achieved.
The immune status of animals was assessed by unified tests (F.Y. Garib et al., 1995; M.V. Zalialieva, 2004). Population composition of lymphocytes in peripheral blood was determined with the help of monoclonal antibodies (LLC Sorbent Service, Moscow) to differentiating surface markers CD3, CD4, CD8, CD16, CD20 and CD95 by indirect blood rosetting. Phagocytic activity of neutrophils (FAN) was determined with latex particles with a diameter of 2.3 microns.
Immune status studies in rats of this group were performed on days 3, 6, 10, 17 and 24.
Results of the study: on the first day of reproduction of the experimental burn in animals, the stress chain of induced pathological disorders (lethargy, adenomia, apnea, tachycardia, polydipsia and uremia) were observed, which allows them to be regarded as a burn disease. On day 3 after excision of the necrotic scab formed, the surface of the burn wound was covered with a gauze cloth moistened with saline solution with gentamycin.
Burn injury in animals caused a change in the immunological reactivity of the organism. On day 3 after reproduction of burn disease in animals, significant disturbances in the state of the immune system were determined, in comparison with the control, which were expressed in a change in the level of quantitative and functional indices of the immune status. Thus, in comparison with the control, a decrease (at P < 0.05) of the relative content of T-lymphocytes (CD3 +) by 32%, i.e., to 35.0 ± 0.81%.
The change in the number of subpopulations of T-lym-phocytes (CD4 + and CE8 + cells), despite a significant decrease of 31% and 27% (to 23.1 ± 0s4% o and 11.8 ± 0.47%, respectively), a violation of their ratio is not it was determined that the immunoregulatory index (IRI) did not differ from the control.
The change in the humoral link of the immune status of animals with Of burn disease was reflected in an unreliable increase in the percentage of B-lymphocytes (CO20 + cells), but was within the control values.
In animals with Of burn disease from 3 days, a significant development of the apoptosis process was revealed, which was
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expressed in an increase in CD95 + cells by 26% (up to 20 ± ± 1.46% versus 15.8 + 0.3% in the control). An increase in the percentage of cells with receptors for apoptosis coincided with a decrease in T-lymphocytes and their subpopulations.
In the early period of burn disease, a significant violation of the state of natural defense factors was determined. With a decrease in phagocytic activity of neytrophenols by 33% (d (up to 31.0 ± 1.36%, with P < 0.05) there was a decrease in the number of phagocytic particles (up to 2.5). This process was accompanied by a slight increase in the percentage of natural killers (CD16 + cells) to 11.0 ± 0.57% versus 10.3 + + 0.33% in the control.
The change in the level of quantitative immunological indices in animals with Of burn disease was determined in their ratio in the dynamics of observation.
By quantitative indices in the state of the T-cell level of immunity on the 6th and 10th days, an insignificant increase in the level of T-lymphocytes and their regulatory subpopulations with a tendency to normalization on days 17 and 24, with preservation of the value, immunoregulatory index (CD4 /CD8) was determined.
In all terms of observation there was an increase in the level of natural killers by 51%, 65%, 65% above control, with normalization towards the end of the experiment (up to 10.6 ±
± 0.49). A significant decrease in the phagocytic activity of neutrophils was still observed, the level of which was 80%, 74%, 75% and 87% at 6, 10, 17 and 24 days, compared with the control. Only by 24 days the increase was 40.5 ± 0.99%, remaining below the control (at P < 0.05).
In the development of burn disease, the animals showed a marked activation of the process of apoptosis of blood leukocytes, which was reflected by an increase in the percentage of CD95 + by 26% -33%, in comparison with the control, at all times of observation.
Thus, it was found that in rats with an induced burn disease, significant violations of the immune status were detected, which were determined by quantitative T-cell and neutrophilic immunodeficiency with increasing natural killers and activation of the apoptosis process.
Conclusions:
1. Induced burn disease in rats promotes changes in immune status in flow dynamics, which are determined by quantitative T-cell deficiency (CD3 +, CD4 +, CD8 + cells).
2. There is a violation of natural protective factors (decreased FAS and increased CD16 + cells) with activation of the apoptosis process (increase of CD95 + cells) in the dynamics of the development of burn disease in the experiment.
References:
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2. Additional diagnostic criteria for severity and prognosis of burn disease. Markelova et al.: method. recommendations.-Vladivostok, 2009.- 19 p.
3. Usov V. V. Assessment of the status of immune status in severely burned // Pacific Medical Journal. 2008.- No. 1.- P. 53-55.
4. Clinical and immunological criteria of burn sepsis. Shlyk and co-authors // Anesthesiology and resuscitation.- M., 2005.-No. 4.- P. 42-45.
5. Quantitative and functional features of the immune status in case of burn disease / Urazmetova MD et al. // Infection, immunity and pharmacology. 2005.- No. 4.- P. 66-69.
6. Dong N. Study on the correlation between CD14 gene polymorphism and T cell-mediated immunity in severely burned patients. Zhonghua Wai Ke Za Zhi. 2009.- Vol. 15. / -sp. 47 (8).- P. 617-620.
