Gut microbiota structure and function can be lastingly altered by short-term extrinsic challenges.
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Expansion of specific organisms can influence collective activities of multispecies communities.
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Switch in activities of the commensal community can trigger dysbiosis.
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Host immune status and interactions of dysbiotic communities instigate destructive inflammation.
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.
