ROLE OF GENETICAL MODIFICATIONS OF FACTORS OF NATURAL IMMUNODEFENCE AT MENINGITIS
DOI:
https://doi.org/10.11603/1681-2727.2016.4.7221Keywords:
meningitis, natural immunodefence, genes, single nucleotide polymorphism.Abstract
Meningitis (M) is a serious life-threatening infectious disease of central nervous system (CNS), which still remains relevance as topical problem of treatment, because it attends with the big percent of complications and residual phenomenons. Inflammatory diseases of CNS can refer to the category of illnesses with a genetical predisposition (multifactorial). The clinical finding of those diseases is formed as a combination of various pathogenetic parts and action of «starting» factors of environment.. Often those pathogenetic parts are damaged by different mutations of genes.
The first line of protection against pathogens is provided by humoral and cellular factors of natural immunodefence which are supervised by genes of the germinal line and don’t variate in the course of the organism life. The most important humoral factors of natural immunodefence are complement, properdin and cytokines. Defects of the genes, which code humoral components of natural immunodefence, lead to disturbances of one of three paths of activation of complement and to development insufficiency of the production of properdin. Effect of those genetical disturbances is the essentiale increasing of susceptibility to meningitis and bacteriogenous infections of Str. pneumoniae, Str. pyogenes, H.influenzae and Neisseria meningitis. As a system of cytokines is polyfunctionality and redundancy, the absence of any cytokine caused by mutations of the conforming genes doesn’t cause catastrophic consequences. The essential role in a nonspecific part of immune system is played by cellular factors - phagocytes. Insufficiency of function of phagocytosis can associated with the genetically conditional reduction of quantity of phagocytes, structurally functional changes of phagocytes, changes of humoral -hormonal regulation of phagocytosis. The recognition of originators by phagocytes has a great value for efective function of natural immunodefence. Recognition of pathogens is carried out simultaneously by several specialised systems of a pattern-distinguishing receptors (PRRs). PRRs are coded by genetically line and aren’t a subject of rearrangement. SNPs in genes of the PRRs lead to generation defective products of recognition and associate with susceptibility to meningococcal and pneumococcal meningitis, as well as TIC-born encephalitis. As a result of intracellular recognition in macrophages and neutrophils there is a formation of the inflamassome, which starts carrying out of the inflammatory reaction. SNPs in inflamassome genes are bonded with adverse outcome of meningitis. As a result of phagocytes activation there is begining of destruction mechanisms of absorbed bacteria. These mechanisms can realized intracellularly and extracellularly, by oxygen-depending and oxygen-independing methods. The most widespread form of disturbance of killing is defect of X-chromosome. Defects of killing set conditions for the relapsing infectious diseases, which are caused by various gram-negative (Escherichia coli, Serratia marcens, Klebsiella pneumonia) and gramme-positive (Staphylococcus aureus) microorganisms.References
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