A new mouse unilateral model of diffuse alveolar damage of the lung.

OBJECTIVE AND DESIGN: The existing biological models of diffuse alveolar damage (DAD) in mice have many shortcomings. To offset these shortcomings, we have proposed a simple, nonsurgical, and reproducible method of unilateral total damage of the left lung in ICR mice. This model is based on the intrabronchial administration of a mixture of bacterial lipopolysaccharide (LPS) from the cell wall of S. enterica and α-galactosylceramide (inducing substances) to the left lung. METHODS: Using computer tomography of the lungs with endobronchial administration of contrast material, we have been able to perform an operative intravital verification of the targeted delivery of the inducer. The model presented is characterized by more serious and homogeneous damage of the affected lung compared to the existing models of focal pneumonia; at the same time, our model is characterized by longer animal survival since the right lung remains intact. RESULTS: The model is also characterized by diffuse alveolar damage of the left lung, animal survival of 100%, abrupt increases in plasma levels of TNFa, INFg, and IL-6, and significant myocardial overload in the right heart. It can be used to assess the efficacy of innovative drugs for the treatment of DAD and ARDS as the clinical manifestations that are developed in patients infected with SARS-CoV-2. Morphological patterns of lungs in the noninfectious ("sterile") model of DAD induced by LPS simultaneously with α-galactosylceramide (presented here) and in the infectious model of DAD induced by SARS-CoV-2 have been compared. CONCLUSION: The DAD model we have proposed can be widely used for studying the efficacy of candidate molecules for the treatment of infectious respiratory diseases, such as viral pneumonias of different etiology, including SARS-CoV-2.

[Autoantibodies to M2-cholinoreceptors as a potential development factor of arrhythmia in patients with paroxysmal atrial fibrillation].

AIM: We aimed to assess autoantibodies to M2-cholinoceptors (M2-CR) in patients with paroxysmal lone atrial fibrillation (AF) and in patients with AF and arterial hypertension (AH). MATERIALS AND METHODS: 100 patients with lone AF and 84 patients with AF and AH were included. Patients underwent clinical blood and urinalysis, assessment of biochemistry blood panel, 12-lead ECG, 24-hour Holter monitoring, echocardiography and stress - testing (treadmill or stress - echocardiography). Assessment of IgM and IgG autoantibodies to M2-CR was performed by indirect immunoenzyme assay. The following peptide molecules were used as epitopes for detection of autoantibodies: M1 - amino acid sequence YTVIGYWPLGVVCDL (83-98) of the first extracellular loop of M2-CR; M2 - sequence VRTVEDGECYIQFFSNAAVTFGTAI (168-192) of the second extracellular loop of M2-CR; M3 - sequence NTFCAPCIPNTV (410-421) of the third extracellular loop of M2-CR; M4 - short sequence VEDGECYIQFFS (171-182) of the second extracellular loop of M2-CR; M1+M4 - chimeric molecule formed by sequences of the first and the second extracellular loops of M2-CR connected by disulfide bound YTVIGYWPLGVVCDL + VEDGECYIQFFS (83-98 + 171-182). RESULTS: Autoantibodies to M2-CR were found in 45% patients with lone AF and in 35% patients with AF and AH. In patients with lone AF prevalence of increased IgG to M2-CR were greater than in patients with AF and AH (32% vs 20%; p.

[Changes in the receptor activity of ß2-adrenoreceptors of human T-lymphocytes under the effect of ß2-agonists].

Changes in the activity of ß2-adrenergic receptors of human T-lymphocytes under the effect of salbutamol (a short-acting ß2-agonist) have been evaluated with a new modified radioligand method utilizing [^(125)I]cyanopindolol and a specific ligand ICI 118551. In healthy volunteers, the receptor activity decreased after 30 min upon the inhalation of salbutamol and restored to the initial level after 2 h. At the same time, there were changes in the transcription level of the ADRB2 gene, which encodes the protein component of the ß2-adrenoreceptor. The dynamics of ß2-adrenergic receptor activity of T-lymphocytes after salbutamol treatment in patients with cardiorespiratory pathology significantly differed from that in healthy volunteers.

[Role of Autoantibodies Against 1-Adrenergic Receptor in Cardiovascular Disease].

According to current knowledge, autoantibodies against 1-adrenergic receptors may be involved in pathogenesis of different cardiovascular diseases and are mostly studied in patients with Chagas disease, dilated cardiomyopathy and heart rhythm disorders. They may play an important role in cardiomyocyte apoptosis, alteration of their chrono- and inotropic effects and electrophysiological characteristics. Their effects are transduced via 1-adrenergic receptors and depend on multiple factors as ligand properties, durability of its coupling with the receptor, amount of receptors on the cell surface, their affinity and conformation. Up to the present moment, reasons for autoimmune response and clinical significance of autoantibodies against 1-adrenergic receptors are not thoroughly understood. Autoantibodies against 1-adrenergic receptors can be removed from the bloodstream by immunoadsorption and thus development of validated methods of their identification is relevant.

[Detection of Autoantibodies Against the 1-Adrenergic Receptor in the Sera of Patients via the Competitive cell-Based Enzyme Linked Immunosorbent Assay].

OBJECTIVE: This study aimed to assess the level of anti-1-adrenergic receptor autoantibodies in patients with ventricular arrhythmias with no signs of organic heart disease and with presence of cardiovascular pathology in comparison with a group of healthy volunteers. MATERIAL AND METHODS: The study included 44 patients with ventricular arrhythmias with no signs of organic heart disease ("idiopathic"), 34 patients with diagnosed dilated cardiomyopathy (DCM) of inflammatory origin, 35 patients with coronary heart disease and ventricular arrhythmias, 12patients with coronary heart disease with no ventricular arrhythmias, and 19 healthy volunteers (control group). The level of autoantibodies against the 1-adrenergic receptor was determined by the developed competitive cell-based enzyme-linked immunosorbent assay (ELISA) and by the standard ELISA using peptides corresponding to the second extracellular loop of the 1-adrenergic receptor. RESULTS: Elevated level of autoantibodies detected by a competitive cell-based ELISA was observed in 62% of patients with DCM compared to 21% of healthy volunteers (p=0.0006). In patients with "idiopathic" ventricular arrhythmias, the level of 1-adrenergic receptor autoantibodies was lower than in healthy subjects (p=0.003). Coronary heart disease patients with or without ventricular arrhythmias exhibited no differences from the control group. The number of significantly positive signals in peptide-based ELISA did not exceed 10% in any of the groups. No correlation between the data from competitive cell-based ELISA and peptide-based ELISA was found. CONCLUSIONS: This study demonstrated that competitive cell-based ELISA technique can be applied for detection of 1-adrenergic receptor autoantibodies. The results in DCM patients generally correspond to the expected. Decreased level of autoantibodies in patients with "idiopathic" ventricular arrhythmias indicates that this disease is related to changes in the immune system. Such relation is not observed in the case of coronary heart disease patients.

[Radioligand Method of Assessment of ß-Adrenoceptor's Activity on Human T-Lymphocytes].

We proposed a new method of evaluation of beta-receptor's activity on the surface of human T-lymphocytes based on the radioligand method. Optimal conditions for evaluation of specific binding to ß2-adrenoceptors of 0.5 fmol ligand per 1 million cells using [125I]-cyanopindolol were found. The possibility of using of ß2-adrenoceptor's activity assessment in clinical settings was demonstrated on human T-lymphocyte.

[Cardiovascular diseases and mannose-binding lectin].

The role of innate immunity factors in the pathogens of ACS is not well studied, although there is evidence in the literature about their impact on the course of cardiovascular diseases. Mannose-binding lectin (MBL)--one of the key factors of the humoral innate immune system that activates one of complement activation pathways. The literature suggests an ambiguous, complex role of MBL, which can in different clinical situations either improve the prognosis of patients, or be a risk factor for complications. MBL could potentially be relevant to all main links in the pathogenesis of coronary artery disease and myocardial infarction: inflammation, thrombosis, apoptosis, and so on. At different stages of atherogenesis, including the formation and destabilization of the atherosclerotic plaque, thrombosis, MBL may have a significant impact. The review analyzes currently available literature on the impact of MBL on atherosclerosis, ischemic heart disease and acute coronary syndrome. Moreover, in the review there is data on the role of MBL in physiological reactions in innate immunity, gene structure of MBL2 and possible mutations leading to deficiency of MBL in blood, and the role of MBL in the pathogenesis of various diseases.

[Level of mannose-binding lectin and phagocytic activity of leukocytes in patients with acute coronary syndrome].

UNLABELLED: Mannose-binding lectin (MBL) is a key component of innate immunity that starts one of the ways of complement activation. Factors of neutrophil activation are cell factors of innate and acquired immunity. AIM: to study MBL levels and factors of neutrophil activation in patients with acute coronary syndrome (ACS). METHODS: A total of 45 patients with ST elevation (STE) ACS and non ST-elevation (NSTE) ACS were enrolled in the study, 15 persons were age-matched controls. RESULTS. Compared with control group MBL level was higher in patients with ACS (52.7 vs 127.2 hg/ml, respectively, p = 0.07), and significantly higher in patients with NSTE ACS (52.7 vs. 164.7 hg/ml, p = 0.03). There was no difference between MBL levels in STE ACS and NSTE ACS patients. Patients with inferior myocardial infarction (MI) had significantly higher MBL level than those with anterior MI (182.8 -92.7 hg/ml, p = 0.02). Patients with concomitant diabetes had statistically higher MBL level than patients without diabetes (225 vs 100 hg/ml, OR 2.25, p = 0.03). MBL level was lower in patients with low (<40%) ejection fraction - 92.7 vs 148.9 hg/ml in patients with EF > or = 40% (p = 0.19). No difference of neutrophil activation factors between ACS patients and controls was found (phagocytic activity of neutrophils 74.5 vs 74.3%, phagocytic number 3.34 vs 4.36, phagocytic reserve 88 vs 85.5 in ACS and control group, respectively). CONCLUSION: Elevated innate immunity factor (MBL) level was associated with ACS, especially in patients with diabetes mellitus. No association between cell immunity factors with ACS was found.

[Estimation of immune response parameters in patients with frequent premature ventricular contractions without signs of organic pathology of the cardiovascular system].

AIM: To study the specific features of an immune response and the role of infectious pathogens in the occurrence, development, and maintenance of ventricular ectopic activity in patients without signs of organic disease of the cardiovascular system (CVS). SUBJECTS AND METHODS: The investigation enrolled 91 patients (27 men and 64 women with a mean age of 36.5 +/- 11.5 years) with premature ventricular contractions (PVC) without signs of organic CVS pathology. A control group comprised 31 healthy volunteers. In addition to standard physical examination, a study of N-terminal pro-brain natriuretic peptide (NT-proBNP) and cellular and humoral immune parameters was performed and the serological and molecular genetic markers of infections were determined in all the patients. RESULTS: The persons with PVC, as compared to the control group, were recorded to have a higher NT-proBNP level (49.2 pg/ml versus 25.4 pg/ml; p = 0.001) accompanied by an increase in both the total number of PVC and the number of coupled PVC and the episodes of ventricular tachycardia. They were also found to have elevated CD3(+)HLA-DR+ (2.4% versus 1.56%) and CD3(+)CD95+ (27.6% versus 18.8%) counts (p = 0.001). In patients with a C-reactive protein level of more than 2 mg/l, the total number of PVC was larger than that in the other patients (p = 0.065). The patients with PVC did not show a statistically significant difference from the controls in the levels of antiviral and antibacterial antibodies. The people with PVC displayed a number of relationships between the infectious pathogen antibody titers and the ECG Holter monitoring and echocardiography readings. CONCLUSION: In the patients with PVC without signs of organic CVS pathology, the parameters of an immune response were not different from those obtained in the control group, which was likely to be associated with the involvement of the immune system in the development and maintenance of ventricular arrhythmias.

[Effect of bosentan on the clinical status and cellular immunity of patients with idiopathic pulmonary hypertension].

AIM: To study the effect of bosentan on the clinical status and cellular immunity of patients with idiopathic pulmonary hypertension (IPH). SUBJECTS AND METHODS: The study enrolled 35 patients with Functional Class (FC) II and IV IPH who had received conventional therapy for 3 months. All the patients took bosentan 125 mg/day for 4 weeks. Then they were randomized to have bosentan 125 or 250 mg/day (Groups 1 and 2). FC was assessed and 6-minute walk test (6MWT), transthoracic echocardiography (EchoCG), and right heart catheterization (RHC) were performed at baseline and after 12 weeks. Peripheral blood lymphocytes were immunophenotyped and the functional activity of neutrophils was determined by their ability to absorb latex particles at baseline and following 3 and 12 weeks. RESULTS: After 12 weeks of treatment, both groups showed a statistically significant increase in the distance covered during the 6MWT. The Borg index and FC also decreased statistically significantly. EchoCG demonstrated a statistically significant reduction in systolic pulmonary artery pressure (SPAP) in Group 1; and in Group 2, SPAP was lower at baseline and remained substantially unchanged (it statistically significantly decreased as evidenced by RHC). Bosentan statistically significantly diminished pulmonary vascular resistance in both groups. No adverse reactions were noted. At baseline, the patients showed a statistically significant elevation in NKT-like lymphocytes up to 10.79 +/- 6.2%. The other indicators of peripheral blood lymphocyte phenotyping did not exceed the normal range. The count of NKT-like lymphocytes remained significantly above the normal levels throughout the follow-up in both groups and slightly dropped in Group 1 patients only after 12 weeks of treatment. In Group 2, the level of CD3+CD25+ lymphocytes rose as compared to the normal levels at 3 and 12 weeks of treatment. At 3 weeks of treatment, there was a statistically significant difference between the groups in phagocytic number. CONCLUSION: Bosentan treatment statistically significantly improves the clinical status of patients with IPH and it is characterized by good tolerability. Bosentan does not exceed the normal count of peripheral blood NKT-like lymphocytes, but it has a direct or indirect positive effect on the B-lymphocytic component of the immune system in patients with IPH.

[Synthetic conformational antigen, simulating the extracellular part of M2-muscarinic receptor and its reactivity with sera from patients with idiopathic arrhythmias].

Linear peptides corresponding to fragment 83-98 of the first loop and fragments 168-192 and 171-182 of the second extracellular loops of M2-muscarinic receptor (marker of early cardiac disorders and arrhythmias) were synthesized by Fmoc-SPPS method. A new conformational antigen was synthesized by method of selective ligation of linear peptides by disulfide bond with native localization. Peptides were studied in reaction with sera from patients with idiopathic arrhythmias. A new conformational antigen was recognized by sera from patients with idiopathic arrhythmias with high reactivity.

[Novel conformational peptide antigen, which simulates an immunodominant epitope of the 2nd extracellular loop of ß1-adrenoceptor. Computer simulation, synthesis, spatial structure].

By means of computer simulation has been built polypeptide antigen conformational structure that imitates the immunodominant epitope of the 2nd extracellular loop of ß1-adrenoreceptor. A linear 25-membered peptide corresponding to calculated sequence was synthesized by means of solid-phase methoyd using Fmoc-technology, then directed by the closure ofdisulfide bridges was obtained original bicyclic polypeptide corresponding to the proposed structure of the conformational antigen. With the help of high-resolution NMR spectroscopy 3D structure of synthetic conformational antigen was investigated. It was shown that the structure of the bicyclic polypeptide similar to that of building computer model. Bicyclic conformational antigen was suitable for the detection of autoantibodies in the blood serum of patients with rhythm and conductivity violation without evidence of organic disease of the cardiovascular system.

[Eosinophilic cation protein and development of restenosis of drug covered stents].

Aim of the study was to assess activation of eosinophils as well as allergic and inflammatory reactions of the body in development of restenosis after implantation of stents with drug covering. We included into the study 32 patients with ischemic heart disease (IHD) and stable angina subjected to repeat coronary angiography during first year after endovascular myocardial revascularization with the help of stents with drug covering, and 11 healthy persons. Levels of eosinophilic cation protein (ECP), immunoglobulin E (IgE), and C-reactive protein (CRP) in blood plasma of patients and healthy persons was determined by immunoenzyme assay. According to results of angiographic study patients were divided into 2 groups: the first comprised 19 patients in whom no instent restenosis was found, the second comprised 13 patients in whom formation of restenosis at least in one stent was noted. Patients in these groups did not differ by age, sex, smokers and nonsmokers ratio, presence of hyperlipidemia, and angiographical characteristics of involved arteries. In patients with restenosis of stents blood plasma ECP level was 17.7 (11.2-24.0) g/ml and significantly higher than in patients without restenosis [9.0 (6.4-12.9) g/ml; p=0.017]. Blood level of IgE in these groups of patients did not differ [58.8 (42.1-164.0) and 52.9 (12.8-76.1) mg/ml, respectively; p=0.40] and did not differ from IgE level in blood of healthy volunteers [32.0 (21.2-80.8) mg/ml; p=0.91]. CRP level in patients with IHD was higher than in healthy volunteers [0.36 (0.1-0.75) mg/ml; p=0.0008)], but did not differ significantly in groups of patients with and without restenosis [2.38 (0.30-4.08) and 1.63 (0.61-2.47) mg/ml, respectively; p=0.52]. It was found that in the group of patients with low blood level of ECP (<11 g/ml) restenoses were revealed in 19% while in the group with higher blood level of ECP (>11 g/ml) - in 62% of cases (p=0,019). In patients subjected to coronary stenting with higher level of ECP in blood we noted more frequent development of restenoses than in patients with low level of this protein. The data obtained allow to suggest presence of relationship between development of restenosis and elevated activity of eosinophilic granulocytes in patients with IHD after revascularization.

[Inflammatory cardiomyopathy: state-of-the-art].

Cardiomyopathy (CMP) is a major cause of early disability and death in young cardiac patients, remaining at the same time a little studied problem. The generally accepted term "dilated cardiomyopathy" is only a portrayal of morphological signs. As of now, the foreign literature most commonly uses the term "inflammatory cardiomyopathy" to denote CMP caused by viral and/or bacterial agents. Owing to the wide use of novel laboratory and instrumental diagnostic techniques, namely: molecular genetic and immunohistochemical studies and endomyocardial biopsy, there has been a possibility to conduct a more accurate and fuller study of inflammatory CMP. Despite the fact that the problems in nosology, classification, choice of the optimal diagnostic methods and management tactics for these patients.

[Effect of steroid therapy on the clinical course of bronchial asthma].

Although only some 5% of the asthmatic population develop severe disease, such cases eat up more than half of the spendings for the management of asthma and they are poorly controlled by the currently available therapies. Most of these patients undergo long-term treatment with various steroid formulations that exert selective action in the airways eliminating one cell type and supporting the growth of another. For this reason, inflammation patterns in severe, as opposed to mild, asthma resemble those in COPD, with a high neutrophil count in the sputum, increased oxidative stress, and poor response to corticosteroids. Such differences in asthma pathogenesis may be due to the accumulation of two CD4+ cell subsets (regulatory T cells and Th17 cells) in the lungs. It is believed that the use of alkylating drugs in low (non-cytotoxic) doses selectively inactivating Tregs and Th17 cells is a promising method for the treatment of severe asthma.

[Characteristics of autoimmune reactions in chronic cardiac failure of different etiology].

AIM: To characterize autoimmune reactions in patients with chronic cardiac failure (CCF) of different etiology. MATERIAL AND METHODS: Basic markers of immune activation were measured in 43 patients with coronary heart disease stage I-IIB (NYHA FC I-IV) and 44 patients with dilated cardiomyopathy (DCMP) stage I-IIB (NYHA FC I-IV). Antibodies to myocardial tissue were studied with indirect immunofluorescence. Echocardiography was made by standard recommendations with evaluation of systolic and diastolic left ventricular function. Concentrations of C-reactive protein, IgG, IgA, IgM were estimated nephelometrically. Enzyme immunoassay studied serum levels of IL-8, IL-2R, IL-6, IL-18, IL-10, IFN-gamma, endothelin. RESULTS: Patients with DCMP had higher titers of antimyocardial autoantibodies than in coronary heart disease (CHD) reflecting more severe autoimmune inflammation. In CHD endothelial, systolic and diastolic dysfunctions severity correlated with severity of inflammation. CONCLUSION: Some characteristics of autoimmune reactions in CCF determine severity of the disease course.

[The study of peculiarities of immunotropic action of statins in chronic heart failure of various etiology].

AIM: To study features of statin therapy in patients with heart failure (HF) of different etiology on immune system. MATERIAL AND METHODS: The basic markers of immune activation in 43 patients with chronic heart disease (CHD) and HF in New York Heart Association (NYHA) class I to IV were studied. Mine age was 48 +/- 8 years (from 33 to 64 years). 43 patients with dilated cardiomyopathy (DCM) and HF were also observed. Mine age was 43 +/- 10 years (from 22 to 61 years). Parameters of systolic and diastolic left ventricle (LV) function were measured. Also non invasive methods for evaluation of endothelial function were used. Concentrations of hsCRP, IgG, IgA, IgM were measured using commercially available kits. IL 6, IL 8, sIL 2R, IL 18, IL 10, IFN Y, endothelin levels were measured using enzyme linked immunosorbent assay method. RESULTS: Statin therapy has immunomodulation effect in patients with heart failure any etiology. This effect depends on etiology of HF. In CHD patients the decreasing of IFN Y, IL 8, sIL 2R, hsCRP and increasing of IL 18, IL 6 levels were observed. In DCM patients the decreasing of IL 8, IL 18, sIL 2R and increasing of IL 10 were observed. There was significant clinical improving in patients with DCM and HF after statin therapy. But there were no changes of endothelial function in patients with CHD and DCM. There were no changes of LV function in patients with CHD. So statin therapy may reduce level of proinflammatory mediators but not fully control inflammation process in patients with HF of different etiology.

[Immune mechanisms of inflammation in dilated cardiomyopathy].

AIM: To study immune mechanisms of inflammation in dilated cardiomyopathy (DCM). MATERIALS AND METHODS: The study of main markers of immune activation was conducted in 44 patients with DCM with stage I - IIB and NYHA functional class (FC) I - IV chronic heart failure (CHF). Among them there were 42 men (95%) and 2 women (5%) in the age from 22 to 61 years. Mean age was 43(10) years. According to FC the patients were distributed in the following way: FC I--10 (23%), FC II--9 (20%), FC III--13 (30%), FC IV--12 (27%). EchoCG was carried out by standard recommendations with assessment of systolic and diastolic function of LV. Measurement of CRP, IgG, IgA, IgM was based on nephelometric method of detection. Content of Il-6, Il-18, Il-10, Il-10, sIl-2R, Il-8, IFN-gamma in blood serum was measured by the method of immunoenzyme analysis. RESULTS: Elevation of levels of CRP, sIl-2R, Il-8 was established in DCM, what evidenced for the presence of inflammatory process. In the group of patients with DCM with rhythm disturbances (predominantly of atrial fibrillation type) elevation of levels of IFN-gamma, CRP was noted what probably was related to Th-1 type of inflammatory reaction. It was revealed that disturbances of diastolic function of the heart had inflammatory genesis (IFN-gamma correlated with parameter of diastolic function DT; elevation of Il-6 level was found in restrictive type of diastolic function). CONCLUSION: Elevation of proinflammatory factors in DCM evidence for the presence of inflammatory process. there exist a link between elevated level of mediators of inflammation and complications of the disease--arrhythmia, worsening of heart failure class, deranged diastolic function of the heart.

[The role of inflammatory factors in pathogenesis of ischemic heart disease].

PURPOSE: To study mechanisms of immune derangements in coronary heart disease (CHD). MATERIAL AND METHODS: We measured basic markers of immune activation in 43 patients with CHD and NYHA I-IV class heart failure (HF). There were 41 men and 2 women aged 33 - 64 years (mean 48 +/- 8 years). Concentrations of hsCRP, IgA, IgM, IgG were measured using commercially available kits. IL-8, sIL-2R, IL-6, IL-18, IL-10, IFN-gamma endothelin levels were measured using enzyme-linked immunosorbent assay method. RESULTS: We found evidence of participation of proinflammatory factors in pathogenesis of HF and established associations of mediators of inflammation (CRP, IL-8) with severity of HF, endothelial dysfunction, and impairment of cardiac function.

[Immunity in chronic bronchitis patients with significant residual changes after prior pulmonary tuberculosis].

To study the immunological features in chronic bronchitis (CB) patients with great residual changes (GRC) after prior pulmonary tuberculosis, the authors examined two groups: 1) 40 CB patients with GRC after prior pulmonary tuberculosis (a study group) and 2) 30 CB patients without a history of pulmonary tuberculosis. The examination revealed that CB patients with GRC after prior pulmonary tuberculosis were found to have higher T lymphocytes, lower B lymphocytes on an exacerbation of the disease. The phagocytic properties of neutrophils were altered as their high phagocytic activity, decreased oxygen-dependent microbicidal activity of phagocytes with their stimulation. The humoral response remained to be slightly pronounced in CB bronchitis with GRC. The low serum levels of TBC active products may suggest the low activity of lipid peroxidation processes in the study group patients. After prior pulmonary tuberculosis, antioxidative activity preserves to be high in CB patients with GRC.