Vol 12, No 2 (2022)

The complement system is the most ancient components in the innate immunity, mainly functioning to primarily eliminate bacterial agents intravascularly. Moreover, the complement complex proteins play a role as a “bridge” between the systems of innate and adaptive immunity providing adequate conditions for maturation and differentiation of B- and T-lymphocytes. The complement system consists of plasma proteins and membrane receptors. Plasma proteins interact with each other via the three described cascade pathways — lectin (which is most ancient phylogenetically), alternative and classical. Lectins are proteins comprising a separate superfamily of pattern-recognizing receptors able to sense molecules of oligo- and polysaccharide nature and induce their aggregation. Among all the lectins, ficolins (FCN) (common domain — fibrinogen) and collectins (common domain — collagen) — mannose-binding lectin (MBL), hepatic and renal collectins have exert unique functions by complexing with carbohydrate components of microbial wall. Formation of a compound complex “microbial wall polysaccharides + collectin/ficolin + specific mannose-binding lectin-associated serine proteases (MARP)” results in the complement system activation, inflammatory reaction and bacterium elimination. Such scenario is proceeded along the lectin pathway compared to the two other pathways called classical and alternative. Examining a role of the complement system and congenital protein defects in the pathogenesis of various diseases is of topical interest because inborn deficiency of the complement components comprises at least 5% out of total primary immunodeficiency rate, whereas the aspects of their prevalence and pathogenesis remain unexplored. Relevance of investigating the complement system components for diverse populations is tremendous, taking into consideration accumulated evidence regarding an important role of the lectin pathway in viral infections. Lectins, the main proteins in the lectin pathway of the complement activation, are encoded by polymorphic genes, wherein single nucleotide polymorphisms (SNPs) result in altered protein conformation and expression, which, in turn, affects functionality and potential to respond to a pathogen. The distribution of the lectin polymorphic gene frequencies and their haplotypes displays extremely marked population differences. According to analyzing available data, population SNP frequencies including those associated with inborn deficiencies for components of the lectin pathway have been currently scarce or unexplored. hence, here we review major lectins and their functions, their functionally significant SNPs in diverse populations and their pathogenetic importance for host defense functions.

Currently, septic shock remains an unresolved public health problem that leads to serious epidemiological, economic and social problems. Septic shock is a common hemodynamic disorder caused by the interaction between pathogenic microbes and host cells, resulting in developing hypoxia, severe metabolic disorders and multiple organ failure. By now, no unified concept for pathophysiology of septic shock are available. However, the aforementioned data prove that one of the key arms in the pathogenesis is endothelial dysfunction and associated ischemic disorders. In the clinical course of septic shock, three stages are distinguished: the stage of compensation, decompensation as well as the stage of irreversible disorders. The initial stage, or the stage of compensation, is characterized by the activated inflammatory response against infectious agents. Clinically, this stage is characterized by the development of “warm shock”: fever, dermal hyperemia, hyperventilation, increased cardiac output, and tachycardia. The second stage in developing septic shock is characterized by arising “cold shock” as a consequence of escalating heart and respiratory failure. The final stage is the development of multiple organ failure manifested by emerging “shock” organs. Multiple organ failure occurs due to microthrombosis and increasing ischemia, which leads to hypoxia and development of mitochondrial dysfunction in immune cells. At this stage patients are characterized by the progressive cyanosis, developing anuria and intestinal obstruction, as well as altered mental status. Laboratory and instrumental diagnostics of septic shock is a promising approach to examine septic shock. The level of serum C-reactive protein, lactate, and proinflammatory cytokines are not highly specific diagnostic parameters of septic shock, because they can be found in any inflammatory process. Today, the promising diagnostic markers are pentraxin-3, high-density lipoproteins, and phosphatidylcholine. The severity of septic shock can be assessed by determining blood schistocytes, central venous pressure, and the ratio of venous-arterial CO₂ and arterial-venous O₂ pressure. The following diagnostic methods can be used to determine multiple organ failure: level of serum proenkephalin A119–159 and heparin-binding protein; echocardiography, troponin I concentration and N-terminal pro-b-type natriuretic peptides; measuring activity of the renin-angiotensin-aldosterone system. Here we discuss the key aspects of pathogenesis, clinical picture and morphological changes of septic shock. The promising methods for diagnosing the disease and its complications have been studied.

In case no assessment of changes in incidence rate can be used as an indicator for effectiveness of applied live plague vaccine, it is really necessary to search for other, particularly immunological correlates for vaccine-based protection. The aim of this study was to reveal immunological correlates for plague protection in mice immunized with Yersinia pestis EV NIIEG, and assess dynamics changes in select markers of plague vaccinated subjects. BALB/c mice were immunized with Y. pestis EV at dose of 2 × 10², 1 × 10³, 5 × 10³, 2.5 × 10⁴ CFU, and on day 21 they were challenged with Y. pestis 231 at a dose of 400 LD₅₀. Immunogenicity was calculated by the Kerber method and ImD₅₀ was determined. Volunteers — 20 subjects who were first vaccinated with live plague vaccine and 20 subjects who were not vaccinated against the plague. Blood cytokine production was measured on the LAZURIT analyzer (Dynex Technologies, USA) in mouse groups before Y. pestis 231 infection on day 14 as well as 21 days after vaccination, in humans — before vaccination, 1, 6 and 12 months after vaccination. The immunized mice showed a significant increase (by 2.2 times) in the induced production of IFNγ and a moderate increase in the concentration of TNFα, IL-10 and IL-17A on day 14 of disease. A high correlation was found between the survival rate of animals and the level of antigen-/mitogen-induced IFNγ production (r = 0.94, p = 0.039), both on day 14 and 21, as well as a noticeable relationship with the level of produced IL-10 and IL-17A on day 14. One month after vaccination volunteers had significantly increase by month 6 (p < 0.05) levels of IFNγ, TNFα, IL-10, IL-17A, although only for IFNγ and IL-17A, the persistence of induced production was noted at a fairly high level for up to a year. Thus, IFNγ and IL-17A can be considered as possible informative correlates of mouse protection against Y. pestis on days 14 and 21, considering the increase in the induced production of these cytokines as adequate markers of the protective efficacy of immunization, and assessing dynamics in these parameters of volunteers vaccinated with the plague live vaccine, the increase in the levels of IFNγ and IL-17A can be considered as a favorable prognostic marker of the immunological efficacy of the vaccine in the period from the month 6 to 12 of observation.

Introduction. Infective endocarditis is a bacterial disease. Pathogen is localized mainly on heart valves and endocardium. This condition is accompanied by immunopathological manifestations and potential generation of septic process being unfavorable prognosis for disease outcome. Currently, the causes of death of patients with endocarditis have been increasingly presented as thromboembolic complications, which severity depends on variant of the disease course. An important role in imbalanced immune system in the infectious process is assigned to altered intercellular interaction mediated via cytokine network. Activated immune cells produce cytokines, which investigating is important in terms of interpreting changes in immune system functionality, assessing the severity of diseases and controlling therapeutic effectiveness. Infective endocarditis remains a severe disease associated with high mortality despite current advances in diagnostics and treatment. A timely diagnostic process and early initiation of treatment are major factors for successful patient management necessitating to improve diagnostics of various clinical variants of endocarditis course, taking into account pathogenetically relevant cytokines. Objective was to comparatively evaluate the importance of serum cytokine concentrations in patients with uncomplicated course of infective endocarditis and its thromboembolic complications and determine cytokine markers of various variants of endocarditis course. Materials and methods. An immunological examination of 119 blood serum samples from patients with confirmed diagnosis of infectious endocarditis and 20 samples from apparently healthy persons was carried out. Depending on the clinical disease form, the patients were divided into 4 groups: group 1 — primary infective endocarditis (PIE) with thromboembolic complications (n = 24), 2 — PIE without thromboembolic complications (n = 34), 3 — secondary IE with thromboembolic complications (n = 27), 4 — secondary IE without thromboembolic complications (n = 34). The control group consisted of 20 apparently healthy subjects. Immunological studies of serum cytokine concentrations were conducted in all groups. Results. Statistically significant increase in serum concentration of IL-10, IL-6, VEGF-A, IL-18, IL-1Ra and IL-8 was revealed in all clinical groups of patients compared to those in control group (p < 0,05). By correlation analysis, we found a significant positive relationship between IL-10 and IL-18 or IL-6. An increase in the concentration of IL-10 leads to increased level of pro-inflammatory IL-18 and IL-6. The marker of secondary endocarditis was observed as increased level of serum concentrations of IFNγ. A characteristic feature of primary infective endocarditis with thromboembolic complications was revealed as significantly increased serum concentration of IL-8, IL-1Ra and IL-6. Markers of secondary complicated endocarditis were identified as increased level of IL-6, VEGF-A and IL-18.

β-defensin-2 (HBD-2) is a peptide of innate immunity that provides the first defenсe line in the oral mucosa against invading pathobionts. Under inflammatory conditions, epithelial cells and gingival fibroblasts produce HBD-2. The defective defensin secretion may play a crucial role in the development of inflammatory periodontal diseases. The study was aimed at comparing HBD-2 levels in the gingival fluid and/or periodontal pockets in patients with dental plaque-induced gingivitis (PG), aggressive periodontitis (AgP), chronic generalized periodontitis (CP) and in the periodontally healthy subjects (Control). We examined 142 patients (45.0±1.03 years) residing in Moscow, including 11 patients with PG (35.7±3.69 years), 43 patients with AgP (35.4±0.84 years), 71 patients with CP (54.4±0.86 years) and 17 controls (36.1±2.92 years). We assessed the periodontal tissue condition in all patients during the periodontal and X-ray examination. The samples of the gingival crevicular fluid and periodontal pocket contents were collected from the gingival sulcus and periodontal pockets at 8 teeth of both jaws by paper points. The concentration (C) of β-defensin-2 was determined by enzyme immunoassay (ELISA Kit for Defensin Beta 2, Cloud-Clone Corp., USA). Mann–Whitney U-test (U), the Kruskal–Wallis test (H) and the Dwass–Steel–Critchlow–Fligner post hoc test (W) analyzed a difference significance between the parameters. We estimated the parameter relationship and its power by using the Spearmanʼs rank correlation coefficient (r_S). The critical significance level was p ≤ 0.05. The current study showed that the progression of the periodontal inflammation is accompanied by sharply decreased HBD-2 concentration in patient samples (H = 42.8, df = 3, р < 0.001). Thus, the concentration of HBD-2 in the gingival crevicular fluid of the periodontally healthy subjects (control group) ranged from 225 to 1720 pg/ml (C = 738 [477; 1114] pg/ml). In patients with PG, the median value of peptide concentration was 242 [42.5; 610] pg/ml (C_min = 19 pg/ml, C_max = 1000 pg/ml). In patients with periodontitis, it declined to critically low levels: C_AgP = 54 [3; 195] pg/ml (C_min = 0, C_max = 478 pg/ml) and С_СP = 25.5 [0; 125] pg/ml (C_min = 0, C_max = 298 pg/ml). Thus, we can consider the level of HBD-2 in the gingival crevicular fluid as a potential predictor for developing inflammatory periodontal diseases.

Helicobacter pylori is considered an etiological agent of chronic gastritis and a number of other diseases of the gastrointestinal tract. The immune response to H. pylori is characterized by the development of both pro-inflammatory and tolerogenic reactions. Against this background, the possibility of forming autoimmune shifts is also assumed. The purpose of the present study was to conduct a comparative analysis of the state of immunity in patients with chronic gastritis in the exacerbation stage associated with and not associated with H. pylori infection. There were used whole peripheral blood (n = 50) and serum (n = 49) samples from 162 patients with primary chronic gastritis at the exacerbation stage, in which the presence or absence of H. pylori DNA was tested by real-time PCR in gastric juice. In the peripheral blood of patients, the relative content of CD4⁺FoxP3⁺ cells (T regulators) and CD4⁺CD161⁺ cells (IL-17 producing cells) was evaluated using flow cytofluorometry and monoclonal antibodies method, the level of mRNA FoxP3 and mRNA IL-17A was determined using real time RT-PCR, and the concentration of IL-2 and IL-23 was determined using enzyme immunoassay. It has been shown that in H. pylori-infected patients with chronic gastritis in the exacerbation stage in comparison with patients not infected with H. pylori, the content of CD4⁺FoxP3⁺ cells, CD4⁺CD161⁺ cells does not change in the blood, also with the level of mRNA FoxP3 and mRNA IL-17A. Since the equilibrium between the populations of Th17 cells and T regulators is modulated by IL-2, which is important for generating the population of T regulators, but inhibits polarization of the immune response towards Th17 cells, we conducted a comparative assessment of the serum IL-2 level in patients with chronic gastritis. All patients showed an increase in IL-2 content in comparison with the norm. In this case, the concentration of IL-2 in the blood of infected H. pylori patients was statistically significantly higher than in H. pylori-uninfected patients. An important regulator of the function of Th17 cells is also IL-23, which induces the differentiation of naive T lymphocytes into Th17 cells involved in inflammatory and autoimmune reactions. In this regard, we determined the level of this cytokine in the blood of patients with chronic gastritis. Multiple increase of IL-23 concentration in comparison with normal level and higher content of IL-23 in H. pylori-infected patients in comparison with uninfected patients were revealed. On the basis of the obtained data, it can be concluded that an increase in the concentration of IL-23 does not exclude the possibility of forming autoimmune shifts with its participation in persons with helicobacter infection, but the issue requires further study.

In the modern world, obstructive jaundice caused by developing a malignant disease — cholangiocarcinoma, poses a significant medical and social problem in economically developed and in developing countries. The aim of this study was to examine parameters of cellular and humoral immunity in patients with obstructive jaundice caused by cholangiocarcinoma before and after surgical intervention. There were enrolled 56 patients with obstructive jaundice caused by cholangiocarcinoma (stages T_2-3N_0-1M₀) and 90 age-matched apparently healthy volunteers. Cellular immunity parameters were studied by using an FC500 flow cytometer (Beckman Coulter, USA). The parameters of humoral immunity were assessed by measuring level of serum immunoglobulins A, M, G, E by using enzyme-linked immunosorbent assay kits manufactured by Vector-Best (Russia). The results were statistically analyzed using the Statistica v. 12.0 software (StatSoft Inc., USA). According to the study results, in patients with obstructive jaundice caused by cholangiocarcinoma, there was revealed activation of humoral immunity due to increased serum level of IgA, IgG, IgE with a profoundly depressed some arms of cellular immunity contributing to the imbalanced work of the entire immune system. The imbalance in the cellular arm of immune system was manifested by decreased count of T helper and increased cytotoxic T cell subsets as well as decline in the CD4⁺/CD8⁺ T cell ratio. An increased count of cytotoxic T lymphocytes points at lowered T cell immunity and existence of a cytotoxic effect at the cellular level. A decrease in the count of pan-marker-positive T lymphocytes indicates about generally reduced activity of the T cell arm due to altered T cell function and, as a result, affected antigen-presenting function in immune cells. The development of T cell immunodeficiency due to T-cell apoptosis confirms upregulated expression of immunomarkers CD38⁺, CD95⁺. An increased serum level for some immunoglobulins suggests developing imbalance in the humoral immunity, whereas rise in the circulating immune complexes indicates about pronounced body intoxication caused by obstructive jaundice due to hyperbilirubinemia and disintegration of tumor cells. Application of surgical correction of obstructive jaundice contributed to normalizing parameters of cellular and humoral immunity, resulting in immunocorrective effect.

Urinary tract infection (UTI) is one of the urgent problems in pediatric nephrology and pediatrics. Despite numerous works devoted to the study of pathogenetic mechanisms and development of new diagnostic measures in patients with urinary tract infection, many questions on pathogenesis have not yet been clearly elucidated. Considering that non-specific symptoms prevailing in the disease clinical picture in children of the first three years of life, it is necessary to search for reliable, early, non-invasive methods for diagnosing urinary tract infections. Purpose of the study is to determine diagnostic and pathogenetic significance of proteins that bind fatty acids as well as zonulin in diagnosis of urinary tract infection in children of the first three years of life. Materials and methods. There were examined 120 children, aged from 29 days of life to 2 years 11 months and 29 days inclusive with urinary tract infection. Control group — 30 healthy children. All children were tested for serum level of proteins that bind fatty acids L-FABP and I-FABP, and the level of I-FABP, L-FABP and zonulin was measured in urine by enzyme-linked immunosorbent assay. Results. In the blood serum of children with urinary tract infection, the levels of L-FABP and I-FABP were significantly increased compared with those in children of the control group (L-FABP — 753.94±26.16 ng/ml vs. 148.7±19.6 ng/ml, I-FABP — 92.97±1.41 ng/ml vs. 18.03±3.03 ng/ml, respectively, p < 0.001). Fractions of urine proteins L-FABP and I- FABP in sick vs. healthy children were also determined at a higher level (6.96±0.19 ng/ml and 1.01±0.25 ng/ml vs. 0.37±0.01 ng/ml and 0.1±0.02 ng/ml, respectively, at p < 0.001). The level of urine zonulin was increased (2.84±0.12 ng/ml) in sick vs. healthy children (0.17±0.04, p < 0.05). Conclusion. The study allowed to identify early markers of kidney and urinary tract damage (L-FABP, I-FABP, ZO) involved in developing inflammatory bacterial process, whereas measuring urine I-FABP, L-FABP, zonulin level can be used for non-invasive UTI diagnostics in infants and young children.

This article is dedicated to analyzing epidemiological situation of Crimean-Congo hemorrhagic fever in the subjects of the North Caucasian Federal District (from 2005 to 2021) and developing a new approach to improve epidemiological forecasting by using an in-progress «prognostic» model. The study is comprehensive, using epidemiological methods and mathematical statistics. The epidemiological analysis was carried out based on information from the databases on the incidence rate for Crimean-Congo hemorrhagic fever presented as a project and maps of infectious disease focus epidemiological examination. The «prognostic» morbidity model is developed based on Bayes’ theorem and Wald’s sequential statistical analysis. The factors information calculation was carried out by using the Kullback method. The value of climatic factors was retrieved from the database of the Center for Collective Use “IKI-monitoring” of the Space Research Institute of the Russian Academy of Sciences. The data obtained indicate that the majority of patients with Crimean-Congo hemorrhagic fever within the studied long-term period in the Stavropol Territory (629) and the Republic of Dagestan (46) were revealed. Isolated cases in the Kabardino-Balkarian Republic (2), the Karachay-Cherkess Republic (3) and the Republic of Ingushetia (2) were noted. Infection by the Crimean-Congo hemorrhagic fever causative agent via the transmission mechanism occurred mainly during the care after farm animals in 59.4%. The prevalence of moderate forms of Crimean-Congo hemorrhagic fever (79%) was noted, with hemorrhagic manifestations (over the last five years) observed almost in half of the patients. The proportion of correct preliminary diagnoses during patient hospitalization was 49%. While testing the «prognostic» model in 2021 particularly in the Stavropol Territory, a complete exact coincidence for predicted and the actual data was obtained for 11 districts (42.3%). False positive (38.5%) and overestimated (11.5%) data at this stage of the study do not significantly reduce the predictive value of the model, since they often reflect registered infection case that occurred at the patient’s place of residence in another administrative region, underdiagnoses of mild forms of Crimean-Congo hemorrhagic fever in medical institutions or high efficiency of preventive measures against ticks measures carried out before the beginning of the epidemic season in individual municipal districts. False negative results were 7.7%. Thus, the results of the analysis evidence about a need to improve the training of medical personnel for the timely detection of patients with Crimean-Congo hemorrhagic fever and to enhance the effectiveness of preventive measures against ticks. The results of testing the “prognostic” model confirm the feasibility and hold promise to continue the study.

Lower respiratory tract infections are among the most important causes of morbidity and mortality in the pediatric population worldwide. Despite advances in treatment and prevention, childhood pneumonia is the major reason for hospital admissions and remains a leading cause of death claiming an estimated 800 000 children’s lives in 2018. Globally, over 1.23 million children died of pneumonia before reaching their 5^th birthday — the equivalent of over 3400 deaths per day worldwide. There is growing evidence that vitamin D plays an important role in the immune system by modulating both innate and adaptive immunity. Vitamin D is an additional factor in the inflammatory response regulation. Its action is mediated via the vitamin D receptor (VDR), which is present in almost all types of immune cells, including activated CD4⁺ and CD8⁺ cells, B cells, macrophages, neutrophils and dendritic cells. Vitamin D deficiency is associated with decreased host defenses against infections. Therefore, our aim was to investigate whether low vitamin D status was a risk factor for pneumonia complications, usage of multiple antibiotics and prolonged hospital stay among hospitalized pediatric patients with community-aquired pneumonia. Total of 200 children (102 healthy controls and 98 with severe pneumonia) from 11 days to 17 years old were included in the study. Cases with severe pneumonia were subdivided into groups with and without complications (36 and 62, respectively). Electrochemiluminescence immunoassay was used to measure the serum 25-hydroxyvitamin D levels. The control group showed lower values than the study group. Cases with complicated pneumonia had significantly lower levels whitin the range of 29.7–68.0 nmol/l, compared with 49.1–88.6 nmol/l in cases without complications. A significant negative correlation was found between vitamin D concentrations and duration of hospital stay, the number of antibiotics used for treatment, and serum levels of inflammatory markers. The low status of vitamin D is related to the severity of the disease but has not been associated with the incidence/frequency of the disease. Children with low vitamin D levels may be at higher risk of developing life-threatening complications, intensive care admissions and a higher inflammatory response.

Micromycetes spp. have been increasingly involved in the etiology of infectious diseases guiding to consider them not as important as bacterial and viral pathogens. Nowadays, a lot of severe forms of candidiasis are caused by C. auris, C. albicans, whereas C. glabrata and C. krusei are of similar importance. Members of these species were selected to investigate related metabolite action on human skin fibroblasts. Candida spp. being continuously found on the epithelium and mucosal membranes resulting in to sustained interaction between microbiota and human cells. Potential to produce metabolites containing pathogenicity factors is one of the crucial events for transition to invasive candidiasis, wherein human epithelial cells build up the front line of defense barrier preventing Candida spp. invasion into deeper host tissues. The study was aimed at assessing data on metabolite effects derived from epidemiologically relevant Candida spp. on primary human skin fibroblast culture in vitro. In particular, there were analyzed Candida spp. metabolites acting on fibroblast monolayer integrity and viability in cell suspension. It was found that Candida spp. metabolites might directly cause fibroblast death so that biocidal activity was exhibited as a strain-specific feature. A direct biocidity against dermal cells was more typical for strains C. glabrata и C. krusei, less pronounced for C. albicans and very weak for C. auris. In addition, a mechanism for secretory product-related biocidal activity derived from various Candida spp. on dermal fibroblasts in vitro revealed that it resulted in fibroblasts death 1 hour after exposure that peaked at 3 hrs. Cell death was equally proceeded via apoptosis and necrosis. Of note, biocidal effect of fungal metabolites showed no correlation with Candida-related potential to cleave intercellular junctions. It was found that C. auris metabolites showing weak biocidity against some fibroblasts simultaneously resulted in more marked disruption of cell monolayer compared to other Candida spp. Perhaps, it is just a feature of C. auris that might account for its higher invasiveness potential allowing to destroy tight human tissues more effectively compared to other Candida spp.

Toxocariasis is a human helminthic invasion that has a wide range of hosts with epizootic distribution. The populational seropositivity in countries with a temperate climate comprises about 37%, whereas in regions with tropical climate — up to 92%. Almost all age groups of the population are at risk of invasion by toxocars. The immunological method currently retains diagnostic significance for toxocariasis, because the reaction of immune system against helminths is accompanied by developing sensitization, and techniques as well as methods of collecting clinical material to identify the migratory form of toxocarosis in humans are time-consuming and invasive. The purpose of this study is to develop an immunobiological preparation based on excretory-secretory antigens from Toxocara canis larvae for serodiagnostics of larva migrans syndrome in human by using enzyme-linked immunoassay (ELISA). Antigens were obtained from Toxocara canis larvae by culturing its eggs isolated from the uterus of female nematodes in the glutamine-supplemented medium. The preparation was purified from ballast substances by centrifugation at 8000 g for 20 minutes followed by filtration through microfiltration membrane with a pore diameter of 0,05–0,15 microns, type MFAS-P-1 (manufactured by CJSC STC Vladipor). Blood serum of student volunteers from countries with high incidence rate of toxocariasis were tested to detect T. canis-specific antibodies. ELISA with commercial antigens Toxocara-IgG-ELISA-BEST kit was used for selection of seropositive and seronegative sera also used as a control. Diagnostic antigenic preparations with different protein concentrations were prepared to examine seropositive sera for determining optimal dose of the antigenic drugs. Results. ELISA with standard test kit allowed to detect Toxocara-IgG antibodies in 20 sera (8%) from 250 samples, what indicates about antigenic stimulation of the immune system by helminths and suspected former disease. Analyzing experimental samples allowed to find the number of seropositive data correlated with antigenic protein concentration in preparations: at a concentration of 1,96 μg/ml 5,2% of positive results were detected, 1,71 μg/ml — 3.2%, 0.33 μg/ml — 0.8% (Pearson’s correlation coefficient 0,94). The number of positive sera detected with commercial antigen in ELISA kit was identical to that of positive sera detected by an experimental antigen sample with a protein concentration of 2,49 μg/ml. Thus, the immunodiagnostic preparations obtained by the experimental method based on the excretory-secretory antigens from Toxocara canis are characterized by high sensitivity and can be used to detect Toxocara-IgG antibodies in ELISA. The antigen preparation protein concentration of at least 2.49 μg/ml is optimal and correlates whit sensitivity of the commercial antigen of the standard ELISA.