[Cellular and molecular mechanisms of interaction between the neuroendocrine and immune systems under chronic fatigue syndrome in experiment].
One of the main mechanisms of chronic fatigue syndrome development involves disturbances of interaction between the immune and neuroendocrine systems. The adequate experimental model for the search of these mechanisms is induction of fatigue in animals via the single intraperitoneal administration of synthetic double-stranded RNA - Poly I : C. Investigation of alterations in cytotoxic and proliferation activities of splenocytcs, the intensity of immunomodulatory cytokines signaling via the sphingomyelin pathways in membrane P2 fraction of the brain cortex, as well as the activity of hypothalamic-pituitary adrenal (HP A) axis in the dynamics of chronic fatigue syndrome in rats has performed. Inhibition of both cytotoxic and proliferative activities of splenocytes during the period of fatigue development has been shown. Priority data concerning the suppression of the activity of neutral sphingomyelinase (nSMase) - the key enzyme of the sphingomyelin cascade - in membranes ofthe cells from the brain cortex on the 3d day after Poly I : C administration to rats have been obtained. It was found that Poly I : C injection to rats led to disturbed HPA axis functions which was manifested by decreased corticosterone concentration in standard functional assays with ACTH and hydrocortisone administration. It is suggested that disturbances in interaction between the immune and neuroendocrine systems during development of chronic fatigue syndrome, including alterations in HPA axis activity, are realized both on the level of changes in the activity of immune-competent cells and immediately on membranes of the brain cells.
Rybakina
E G
EG
Shanin
S N
SN
Fomicheva
E E
EE
Korneva
E A
EA
D000324:Adrenocorticotropic Hormone / Q000276:immunology / Q000494:pharmacology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000276:immunology / Q000494:pharmacology; D000998:Antiviral Agents / Q000009:adverse effects* / Q000494:pharmacology; D002462:Cell Membrane / Q000276:immunology; D003345:Corticosterone / Q000276:immunology; D015673:Fatigue Syndrome, Chronic / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D005260:Female; D006728:Hormones / Q000276:immunology / Q000494:pharmacology; D006801:Humans; D006854:Hydrocortisone / Q000276:immunology / Q000494:pharmacology; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology*; D010913:Pituitary-Adrenal System / Q000276:immunology*; D011070:Poly I-C / Q000009:adverse effects* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology; D013108:Sphingomyelin Phosphodiesterase / Q000276:immunology; D013109:Sphingomyelins / Q000276:immunology; D013997:Time Factors
D000893:Anti-Inflammatory Agents; D000998:Antiviral Agents; D006728:Hormones; D013109:Sphingomyelins; D000324:Adrenocorticotropic Hormone; D013108:Sphingomyelin Phosphodiesterase; D011070:Poly I-C; D003345:Corticosterone; D006854:Hydrocortisone