Concommensal microbiotas influence cerebral function, emotions and reactions of the body's immune system to severe stresses (ACTH and corticosterone). Little is known about the function of microbiotas in the design of chronical stressful reactions in the peripherical constituents of the hypothalamus-pituitary gland epinocortical axes (HPA) and in the large intestine. Here we were studying the effects of chronical pressure-Mikrobiota interactions on HPA midline activity and on the term of the coloric corticotropin-releasing HRH (CRH) system, the cytokines receptor and 11?-hydroxysteroid dehydrogenase class 1 (11HSD1), an enzyme that detects locally produced glycocorticoids.
We were able to show with SPF and GF BALB/c biomice that the micobiota modulated emotions in the course of societal conflict and the reaction of the HPA axes, the large intestine and the mesenteriallymphnodes ( "MLN") to chronical psychological distress. While in the hypophysis it weakened the activity of Fkbp5, a protein that regulates the sensibility of the glycocorticoid receptors, in the suprarenal glands it weakened the activity of steroidogenicity ( (MC2R, StaR, Cyp11a1) and the production of catecholamines (TH, PNMT) coding for the production of steroids.
Hypophyseal activity of CRH1 ( "CRHR1") receptors and protomelanocortin was not affected by microbiotas. Microbiotassium decreased 11HSD1, CRH, UCN2 and its CRHR2 receptors in the large intestine, but increased the levels of cytokine activity in the large intestine ?, IL-4, IL-5, IL-6, IL-10, IL-13 and IL-17, with the exceptions of IL-1?.
In comparison to GF rats, chronical stressed uploaded in SPF phage in SPF regulated the expressing of Fkbp5 and colon CRH and UCN2 and dowregulated the expressing of colony cytocines. Disparities in the stressful reactions of GF and SPF animal were also found in the analysis of the immune phenotype of MLN cell and its cytokine excretion.
Evidence suggests that the existence of microbiota/intestinal comminals is important in determining the reaction of surrounding tissue to stresses and indicates possible ways in which the enviroment can react with glucocorticoids signals.