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Biomedical subjects

V A Nagornev

Publications and source records attributed to V A Nagornev.

At least 19 recordsLinked to original sources
PubMed2006

[Contemporary views on the pathogenesis of atherosclerosis].

Recent studies show that inflammation plays the key role inthe pathogenesis of atherosclerosis. Immune cells dominate at the initial stages of the atherosclerotic lesion of blood vessels. The effector molecules accelerate the progress of the lesion. This approach to the assessment of the pathogenesis of atherosclerosis makes it possible to search the ways for the prevention and suppression of immune inflammation. Nowadays vaccination against primary autoantigens is being successfully used for protection from experimental atherosclerosis. Modulation of immune response, involved in atherosclerosis, includes vaccination inducing immune protecting response of the development of tolerance by means of the process from Th1 to Th2 cell response.

Animals↗
PubMed2005

Myocardial tissue damage in rabbits injected with group A streptococci, types M1 and M22. Role of bacterial immunoglobulin G-binding surface proteins.

Acute rheumatic fever (ARF) and acute poststreptococcal glomerulonephritis (APSGN), two important sequelae of streptococcal throat or skin infections, according to current concepts may be elicited by autoimmune mechanisms due to molecular mimicry between group A streptococci (GAS) and human tissue. In the case of APSGN, however, our experimental data have indicated that GAS immunoglobulin-binding surface proteins (IgG BPs) might be of pathogenic significance by triggering anti-IgG production and immune complex formation leading to renal damage. Thus, rabbits injected with IgG-binding, as opposed to non-binding, GAS strains were found to develop renal deposition of IgG and complement factor C3 and inflammatory and degenerative glomerular changes resembling the picture seen in APSGN. In the present study, cardiac tissue material from rabbits injected with GAS was investigated. After 8 or more weeks of intravenous (i.v.) injections, minimal changes were seen in those animals receiving an IgG non-binding GAS strain, type T27, whereas those animals receiving either of two IgG-binding GAS strains, types M1 or M22, developed strong inflammatory and degenerative myocardial changes accompanied by deposition of IgG and C3. Furthermore, on injecting rabbits with defined mutants of a type M22 strain, the development of myocardial tissue damage proved to be dependent on the presence of streptococcal IgG-binding activity. Our results demonstrate that myocardial tissue changes may be induced in the rabbit by i.v. injection of whole heat-killed GAS of at least two M serotypes. Conceivably, induction of immune complexes by bacterial IgG BPs may lead to myocardial deposition of IgG, in turn triggering a series of events, involving the complement system and proinflammatory cytokines, with resulting tissue damage. Though many virulence factors may be involved in the development of ARF and APSGN, and a given GAS strain will never cause both, our results may suggest a new pathogenetic mechanism common to these two major non-suppurative complications.

Animals↗
PubMed2004

Induction of myocarditis in rabbits injected with group A streptococci.

BACKGROUND & OBJECTIVES: We have earlier proposed that group A streptococcal (GAS) immunoglobulin binding surface proteins (IgGBPs) might trigger anti-IgG production and immune complex formation leading to glomerulonephritis. In the present study, cardiac tissue material from rabbits injected with heat-killed GAS was investigated. METHODS: Rabbits were injected intravenously with 10(9) colony forming units of streptococci three times weekly for 8 wk. Cardiac tissue samples were obtained at different times and deposition of IgG, C3, TNF-alpha and IL-6 was studied. RESULTS: After 8 or more weeks of intravenous (iv) injections, minimal changes were seen in animals receiving an IgG non-binding GAS strain, type T27, whereas in those animals receiving either of two IgG binding GAS strains, types M1 or M22, strong inflammatory and degenerative myocardial changes accompanied by deposition of IgG and C3 were noted. Furthermore, on injecting rabbits with defined mutants of a type M22 strain, the development of myocardial tissue damage proved to be dependent on the presence streptococcal IgGBPs. INTERPRETATION & CONCLUSION: The present data supported a role of streptococcal IgGBPs in the induction of myocardial tissue injury by GAS.

Animals↗
PubMed2004

[Atherogenesis as an immunoinflammatory process].

The paper contains findings, obtained at the laboratory of atherosclerosis of Anichkov's Research Institute of Experimental Medicine, Russia's Academy of Medical Sciences, during the last decade with the above research results being compared with published data. Atherogenesis is discussed from the standpoint of the development of immune inflammation in the arterial wall. The mechanisms and factors triggering the chain of immunoinflammatory reactions, which provoke and keep up the inflammatory process, are also under discussion. The results are indicative of that the atherosclerosis pathogenesis is equally related both with mLDL and with the reaction developing in the vascular wall.

Aorta↗
PubMed2003

Cytotoxic effect of low-density lipoproteins.

The cytopathogenic effect of various modified lipoproteins on cultured peritoneal macrophages was studied in vitro. After minor peroxide modification lipoproteins induced apoptosis of macrophages. Immune complexes containing oxidized lipoproteins caused cell necrosis.

Animals↗
PubMed2002

[Current views on the pathogenesis of atherosclerosis from the position of infectious pathology].

The role of immune inflammation at atherogenesis is studied in the paper. Two etiological factors of atherosclerosis pathogeny are under examination: the role of modified low density lipoproteins (mLDL) and essential parasites (Chlamydia pneumoniae and Cytomegaloviruses). Generality of immune response during persistent infection into a blood vessel wall and deposit or formation of mLDL are discussed. The point of view is substantiated that the development of atherosclerotic damages of blood vessels is speeded up by a combination of the two mentioned etiological factors.

Animals↗
PubMed2000

[Atherogenesis as a reflection of immune inflammation in the vascular wall].

Despite numerous basic and applied studies into the pathogenesis and treatment of atherosclerosis, there is no theory which could explain the development of the whole complex of changes united under the term "atherosclerosis". Examining the causes of atherosclerosis disclosed a pathogenetic association of the immunoregulatory signal CD40-CD40L with the occurrence of arterial atherosclerotic lesions. Studies of the immune mechanisms responsible for the pathogenesis of atherosclerosis (autoimmune complexes containing oxidative modification of LDL, T and B lymphocytes, inflammation mediators, hemoadhesive molecules, and immunoregulatory molecules showed the leading role of autoimmune mechanisms in atherosclerosis. The conceptual result of the studies is that the authors have elucidated the leading role of immune inflammation in the appearance and development of arterial atherosclerotic lesions. The development of a new concept of assessing the pathogenesis of atherosclerosis in the context of immune inflammation in the vascular wall opens new vistas for the treatment of this disease.

Arteries↗
PubMed1998

Triggering of renal tissue damage in the rabbit by IgG Fc-receptor-positive group A streptococci.

Our previous studies have shown that streptococcal IgG Fc receptors (FcR) act to elicit circulating anti-IgG as well as renal glomerular deposition of IgG in rabbits immunized with group A streptococci (GAS). In order to study if other FcR-positive bacteria might have similar effects, rabbits were immunized with either group G streptococci (GGS; strain G148) or Staphylococcus aureus (strain Cowan I) for two periods of 8 and 6 weeks, respectively. At the end of immunization, circulating anti-IgG was found in 6 of 20 (30%) and 4 of 19 (21%) animals receiving G148 and Cowan I, respectively, compared to all 28 receiving FcR-positive GAS strains of types M1, M4, M15 or M22 (p < 0.05 for both comparisons); furthermore, anti-IgG appeared earlier and at higher levels in the GAS groups. Weak glomerular IgG deposits occurred in 5 out of 10 (50%) and 2 out of 8 (25%) animals immunized with G148 and Cowan I, respectively. In contrast, all 11 rabbits examined, given GAS of types M1 or M15, displayed heavy deposits. None of four control animals immunized with either of two FcR-negative strains, GAS type T27 or group B streptococci (GBS) type Ia, exhibited any renal IgG deposits or circulating anti-IgG. Renal tissue materials from rabbits immunized with any of the four FcR-positive GAS strains showed strong inflammatory and degenerative glomerular changes, compatible with the picture seen in acute poststreptococcal glomerulonephritis (APSGN). Only transient renal changes were found in those rabbits immunized with G148 or Cowan I, or the controls injected with the FcR-negative strains, GAS type T27 or GBS. Thus, only the FcR-positive GAS strains showed capacity to induce high levels of anti-IgG, pronounced tissue deposition of IgG as well as irreversible glomerular changes. Our experimental data suggest that streptococcal IgG FcR activity might play an important role in triggering APSGN.

Animals↗
PubMed1998

[Endocrine and immune homeostasis in atherosclerosis].

The review analyzes endocrine and immune homeostasis, showing that with aging there is a higher sensitivity to humoral factors and a lower sensitivity to nerve stimuli, thus is why the role of self-regulation, in early atherosclerosis in particular. Endocrine and immune homeostasis is shown to characterize not only the pathological processes in the body, but also to determine the development of immune inflammation in the vascular wall.

Aging↗