Mechanisms of realization of protective effect of miliacin during experimental Salmonella infection: effect of endotoxinemia and cytokine production

• Published in: Žurnal mikrobiologii, ėpidemiologii i immunobiologii no. 5; p. 8
• Main Authors: Frolov, B A, Chaĭnikova, I N, Filippova, Iu V, Smoliagin, A I, Panfilova, T V, Zheleznova, A D
• Format: Journal Article
• Language: Russian
• Published: Russia (Federation) 01-09-2014
• Subjects: Animals; Endotoxins - blood; Gene Expression Regulation; Humans; Inflammation - drug therapy; Inflammation - genetics; Inflammation - pathology; Interferon-gamma - biosynthesis; Interleukin-10 - biosynthesis; Interleukin-12 - biosynthesis; Interleukin-17 - biosynthesis; Mice; Salmonella enteritidis - pathogenicity; Salmonella Infections, Animal - drug therapy; Salmonella Infections, Animal - genetics; Salmonella Infections, Animal - pathology; Triterpenes - administration & dosage
• ISSN: 0372-9311

Evaluate the effect of miliacin on the intensity of endotoxinemia and features of cytokine production in experimental salmonella infection.
The studies were carried out in 128 male mice (CBAxC57Bl6)F1 divided into 4 groups: I--intact; II--infected; III--infected after administration of miliacin solvent: tween-21; IV--infected after administration of miliacin. Determination of the endotoxin in blood plasma was carried out by using chromogenic LAL-test. Cytokine production was studied in splenocyte culture by EIA method.
Miliacin reduced the intensity of endotoxinemia in mice of group IV. Salmonella infection increased spontaneous (IFNγ) and induced (IL-12, IFNγ, IL-17) cytokine production. Miliacin ensured the most significant increase of spontaneous IL-10, IL-12 and IFNγ production compared with groups II and III. At the same time it limited the increase of induced IL-17 production compared with groups II and III.
Protective effect of miliacin is determined by the reduction of endotoxinemia, mobilization of Th-1 response, stimulation of IL-10 production and limitation of IL-17 participation in the development of the inflammatory reaction.