Abstract
To study the effect of thermal trauma on the immune response formation, 43 patients aged 16 to 58 with body surface area of burns 20-60% were examined. The neutrophilic granulocytes (NG) and monocytes functional activity, the content of myeloperoxidase and substances with a positive reaction to Schiff’s periodic acid (PAS- stained substances), the cytokines content were determined: interleukin-1β (IL-1β), IL-2, IL-4, IL- 6, tumor necrosis factor-α (TNF-α). Thermal damage caused changes in the immune response, which were characterized by a pro-inflammatory phase in which innate immunity cells (neutrophilic granulocytes, monocytes) acquired high functional activity, producing a higher content of proinflammatory cytokines. On the 2-3rd day after the burn injury in the peripheral blood, the interleukin-1β (IL-1β) content was 133.5 ± 21.1 pg/ml, the tumor necrosis factor α (TNF-α) content was 265 ± 115.5 pg/ml, which exceeded the reference values by 5.1 and 10.9 times, respectively. The content of IL-6 on the 2-3rd day was 85.30 ± 13.10 pg/ml. Also a concomitant syndrome of compensatory anti-inflammatory response developed with increasing production of anti-inflammatory IL-4: on the 2-3rd day after burn injury, its content was 268.5 pg/ml, exceeding the reference values by 8.2 times. The content of anti-inflammatory IL-10 was decreased. This suggests that anti-inflammatory cytokines do not compensate for the high content of pro-inflammatory factors. On the 7th-8th day after the burn injury, there was a tendency to further increase the content of pro-inflammatory cytokines IL- 1β and TNF-α to 148.0 ± 27.0, and 281.2 ± 146.7 pg/ml, respectively, while the content of IL-6 on the 7-8th day was 131.0 ± 11.1 pg/ml, the anti-inflammatory cytokine IL-10 increased slightly, and the content of IL-4 decreased. These changes in the early period of burn disease dynamics, as well as reduced activity of myeloperoxidase and PAS- stained substances NG, point for a functional deficiency of NG, reduced enzymatic activity and cells energy resources decompensation. These changes could clinically lead to SIRS progression and multiorgan dysfunction.
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