Differences in the pools of 10 cytokine were found in blood samples from the caudal vein of mice with normal and abnormal heart rhythm. Both groups were albino mice bred by us and differing from mdx albino mice by the absence of mutation in muscular dystrophin gene. Mice with normal heart rhythm had low IL-17 content and elevated concentrations of proinflammatory cytokines IL-6 and IL-1α in comparison with the normal (according to published data). In mice with bradyarrhythmias, increased blood levels of IL-10, IL-6, IL-5, IL-2, IL-1α, IL-17, IL-4, TNF-α, and granulocyte-macrophage colony-stimulating factor were detected. The relative content of IL-4 and IL-17 in the total cytokine pool increased. The lifespan of mice with bradyarrhythmias and cytokine hyperexpression was shorter by 2-3 months in comparison with mice without heart rhythm disturbances and moderate changes in the cytokine pool.
In mdx mice, mutation in the muscle protein dystrophin gene results in the development of chronic degeneration of the muscle tissue. We performed a comparative analysis of blood cytokine levels in mdx mice, classical black mice and mice with additional genetic defect responsible for the manifestations of oculocutaneous albinism. In mdx albino mice, the total pool of cytokines (IL-10, IL-6, IL-5, IL-2, IL-1α, IL-4, IL-17, granulocyte-macrophage growth factor, TNF-α, and IFN-γ) was increased. This increase was not associated with selective release of one of the above cytokines into the blood. The fraction of pro-inflammatory cytokines (IL-6, IL-1α, TNF-α) was increased in the total pool and the percentage of antiinflammatory cytokines (IL-4) was reduced. Changes in cytokine pool probably reflect the differences in the severity of the pathological process in the muscle tissue of both genetic variations of mdx mice.
Human embryonic myogenic precursors were transplanted into muscles of mdx mice with hereditary dystrophin-deficient muscular dystrophy. Transplantation induced the synthesis of human dystrophin. The number of dystrophin-positive fibers progressively decreased, however, some of them were preserved even 5 months after transplantation. Our results indicate that xenogeneic transplantation of embryonic myogenic precursors compensates the genetic defect in dystrophin-deficient mice.
A relationship between enteric microbiocenosis and severity of type 1 diabetes mellitus was detected. Microbiological analysis showed II-IV degree dysbacteriosis in all diabetic children. Long-term therapy with probiotics aimed at eradication of opportunistic microflora resulted in recovery of microbiocenosis, which was paralleled by improvement of the clinical status, regression of complications in children who were ill for a long time, and prevention of complications in children with newly detected diabetes. These results indicate the leading role of chronic enteric toxic infectious process in the development of complications of type 1 diabetes. The significance of infection in the pathogenesis of other noninfectious diseases in man is discussed.
Life-time monitoring of the main clinical and laboratory manifestations of hereditary muscular dystrophy in mdx mice confirmed the presence of mutation in exon 23 of dystrophin gene and the absence of this protein in skeletal muscles of mutant animals. Muscular dystrophy in mice was similar to human progressive muscle disorder, which allows the use of this model for the development of cell technologies for the treatment of hereditary muscular diseases in humans.
Multicellular organisms and the saprophytic flora form complex, highly integrated chimeric systems (associative symbioses, metaorganisms) characterized by interplay between pro- and eukaryotic components. To be able to interact symbiotically microorganisms (MO) need a whole body.When grown on artificial media for a long time, symbiotic MO have to adapt to the artificial environment and gradually, though reversibly, lose their ability of associative interaction with the human body, thus causing a decrease in the therapeutic efficacy of MO-derived probiotic products. To increase the therapeutic activity of probiotic MO, they must be functionally rehabilitated.A pathological process induces development of a secondary metabolic dysbiosis; as a result, changes in the regulatory processes of an individual interfere with the restoration of the normal microflora. Therefore, functional rehabilitation of probiotic MO must take place during cultivation, while the cultivation process must replicate the whole-body conditions.
Life-time monitoring of the main clinical and laboratory manifestations of hereditary muscular dystrophy in mdx mice confirmed the presence of mutation in exon 23 of dystrophin gene and the absence of this protein in skeletal muscles of mutant animals. Muscular dystrophy in mice was similar to human progressive muscle disorder, which allows the use of this model for the development of cell technologies for the treatment of hereditary muscular diseases in humans.
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