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Role of microbiota in mouse experimental model of psoriasis
Jirásková Zákostelská, Zuzana ; Stehlíková, Zuzana ; Klimešová, Klára ; Rossmann, Pavel ; Dvořák, Jiří ; Novosádová, Iva ; Kostovčík, Martin ; Coufal, Štěpán ; Šrůtková, Dagmar ; Hudcovic, Tomáš ; Štěpánková, Renata ; Rob, F. ; Jůzlová, P. ; Herzogová, J. ; Tlaskalová-Hogenová, Helena ; Kverka, Miloslav
Anotace v anglickém jazyce\n\nMouse model of human psoriasis and gnotobiotic are important tools in understanding the role of gut and skin microbiota in pathogenesis of psoriasis. In our experiments we showed that gnotobiotic mice, as well as conventional mice treated with antibiotics, have milder skin inflammation in comparison with control conventional mice. Treatment with broad spectrum antibiotics led to dramatic shift in gut microbial composition, in particular, we observed extensive increase of order Lactobacillales. To analyze the potential effect of Lactobacillales on skin inflammation, we further monocolonized mice with L. plantarum WCFS1. Also monocolonized mice showed lower skin inflammation in comparison with conventional mice. To understand whether microbial dysbiosis is cause or effect of psoriasis needs to be further investigated.\n\n
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Immunologic profile of experimental autoimmune encephalomyelitis
Novosádová, Iva ; Fišerová, Anna (advisor) ; Zajícová, Alena (referee)
5 Anglický abstrakt Experimental autoimmune encephalomyelitis (EAE) is widely accepted as a murine model of human multiple sclerosis autoimmune disease. Murine EAE is usually actively induced by immunization with a suitable myelin antigen. Following immunization, CD4+ T helper lymphocytes Th1 and Th17 accumulate in the nervous tissue and via the production of cytokines, they mediate an inflammatory reaction and the subsequent destruction of myelin. The main goal of this study was the induction of EAE with clinically observable symptoms and the observation of changes in the counts and phenotypes of cells, mainly NK and T cells. NK cells express a wide range of inhibitory and activation receptors from the C-lectin-like receptor superfamily. The specific ligand of the activating NKR-P1C isoform is still unknown and thus this receptor's involvement in EAE was also observed. Another goal was the use of medication with regard to the disease progress improvement. For the purposes of this study, two inbred murine strains with distinct NKR-P1 surface expression were used - the SJL/J strain (expressing inhibitory NKR-P1B) and C57BL/6 (expression activating NKR-P1C). SJL mice elicited a relapse-remitting of EAE, while C57BL/6 had chronic EAE. Both mouse strains exerted changes in the counts of NK...
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