Introduction. The complex of unfavorable natural and climatic factors in the North, creating a stressful living environment, induces a pronounced tension in the immune responses that maintain homeostasis. Determining the type of adaptation reaction and the level of reactivity makes it possible to diagnose the functional state of the body and predict its response patterns to environmental factors.

Objective. Determination of systemic inflammation biomarker levels, calculated based on complete blood count data, for assessing the stress and failure of the adaptation process.

Materials and methods. The study examined 178 practically healthy volunteers (136 women and 42 men; mean age 31.17 ± 0.85 years). The assessment of the body’s adaptation state was carried out by analyzing leukograms. The types of non-specific adaptation reactions, levels of body reactivity, and adaptation state were determined according to Garkavi’s method. According to this method, all subjects were divided into the following groups: “physiological norm” (group 1) — 68 women and 23 men, mean age 31.59 ± 1.29 years; “adaptation stress” (group 2) — 50 women and 10 men, mean age 31.21 ± 1.15 years; “adaptation failure” (group 3) — 18 women and 9 men, mean age 28.17 ± 2.51 years. General short-term cold exposure was modeled once in a climatic chamber (USHZ-25N, Russia), in which the subjects, dressed in cotton clothing, remained under continuous video observation for 5 min at an ambient air temperature of –25 °C. Hematological studies were performed using an XS-500i analyzer. The content of catecholamines, cortisol, PPARγC1α, HIF‑1α, SIRT3, and BPI was determined by ELISA. Lymphocyte apoptosis and necrosis were assessed by double staining with Annexin V and propidium iodide (AnV/PI). The quantitative content of ATP was determined using the luciferin‑luciferase method. The following systemic inflammation indices were calculated: systemic immuneinflammation index (SII), systemic inflammation response index (SIRI), and aggregate index of systemic inflammation (AISI). The results were processed using StatTech v.4.9.2 and Statistica 6.0 software.

Results. In the “physiological norm” group, an increase in leukocyte counts, enhanced cell migration activity, and improved mitochondrial energy supply for their functional activity indicated high non-specific resistance and the absence of a stress effect from this type of cold exposure. Under “adaptation stress”, the fastest cardiovascular responses aimed at maintaining temperature homeostasis were recorded, accompanied by increased catecholamine levels, enhanced leukocyte recirculation and migration, allowing the body to respond rapidly to short‑term stress factors. In the “adaptation failure” group, the baseline tension in the activity of regulatory systems, even after a single short‑term cold exposure, did not lead to the activation of effective thermoregulation mechanisms; leukocyte migration activity was slowed, significantly increasing the risk of maladaptive and pro‑inflammatory reactions. It was established that SIRI, SII, and AISI are significant risk criteria for adaptation strain at SIRI ≥ 0.97, SII ≥ 447.43, AISI ≥ 216.24, and for adaptation failure at index values of ≥1.23, ≥449.76, and ≥239.58, respectively.

Conclusions. “Adaptation stress” and “adaptation failure” are characterized by changes in cellular and humoral parameters of peripheral blood even before the clinical manifestation of the disease, and these changes may be exacerbated by additional exposure to negative factors, even if their impact is short‑term. Baseline systemic inflammation indices (SIRI, SII, AISI) are significant predictors for assessing both “adaptation stress” and “adaptation failure”. The use of these indices, calculated from complete blood count results, will make it possible to assess the presence of an initial imbalance in the body’s adaptation mechanisms, which may subsequently be aggravated by exposure to stress factors.