title: Inflammatory disease caused by intestinal pathobionts.
abstract: Environmental and intrinsic factors that alter microbiota structure can trigger aberrant immune responses. The resulting states of dysbiosis take many forms characterized by overrepresentation of pro-inflammatory organisms and pathobionts and loss of beneficial commensals further aggravating the inflammatory state. The pathogenic potential of the dysbiotic community can be linked to specific organisms in some cases but accumulating evidence suggests that intestinal inflammatory diseases are driven by collective functions of highly variable polymicrobial communities. Key challenges are to gain sufficient knowledge of the structure and function of a given disease-causing consortium to understand how inflammation is perpetuated, to identify the protective mechanisms lost in the absence of specific commensals and test interventions to shift a persistent dysbiotic community to a more benign state.
authors.affiliation: Institute of Molecular Biosciences, University of Graz, Humboldtstrasse 50/1, A-8010 Graz, Austria; BioTechMed-Graz, Austria. Electronic address: ellen.zechner@uni-graz.at.
authors.forename: Ellen L
authors.initials: EL
authors.lastname: Zechner
mesh_terms: D000818:Animals; D001419:Bacteria / Q000472:pathogenicity; D016360:Clostridioides difficile / Q000472:pathogenicity; D064806:Dysbiosis / Q000276:immunology; D004751:Enteritis / Q000276:immunology / Q000382:microbiology*; D000069196:Gastrointestinal Microbiome / Q000276:immunology / Q000502:physiology*; D054884:Host-Pathogen Interactions / Q000235:genetics; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000382:microbiology; D007422:Intestines / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D051379:Mice; D059013:Microbial Consortia / Q000276:immunology; D013559:Symbiosis