THE ROLE OF MICROBIOTA IN PATHOGENESIS OF INFLAMMATORY AND NEOPLASTIC DISEASES. CONTRIBUTION OF GERM-FREE MODELS OF HUMAN DISEASES

Recently developed culture-independent methods to characterize the gut microbio­ta has renewed interest in its role in host health and disease. Association was identified between changes in the composition of gut microbiota and the development of diseases, both enteric and systemic. Numerous immu­nologically mediated chronic diseases may occur as a result of disturbance of intestinal microbiota composition („dysbiosis“), impaired mucosal barrier function and changes in im­munoregulating mechanisms.

An irreplaceable role in the efforts to elucida­te the role of microbiota in the pathogenetic mechanisms of inflammatory and neoplastic diseases, is played by gnotobiology. Experi­mental animals as models of human disease (induction of disease or genetically manipu­lated models) reared in germ-free breeding isolators are used for comparison with conven­tionally bred experimental animals (colonized with normal microbiota) for the purpose of mo­nitoring the participation of commensal bac­teria in the development of diseases. Moreover, germ-free animals can be colonized by defi­ned strains of bacteria or by microbiota from patients (“humanized mouse”), and the parti­cipation of microbiota components in the de­velopment of diseases can thus be directly ob­served. Using gnotobiological methods we have shown eg. that gut microbiota transferred from intestinal biopsy samples of patients with IBD promotes intestinal inflammation. Moreover we demonstrated the impact of gut microbiota composition on colitis-associated colon cancer development. Identification microbiota com­ponents, elucidation of molecular mechanisms of their action and efforts to find various means of manipulating the gut microbiota of research animals would aid to develop new approaches in disease prevention and treatment.

Prezentace ke stažení

• Prof. MUDr. Helena Tlaskalová-Hogenová, DrSc. – Tlaskalova_THE ROLE OF MICROBIOTA IN PATHOGENESIS OF INFLAMMATORY AND NEOPLASTIC DISEASES. CONTRIBU