Under or intrinsic factors like host genetics. Nevertheless,

Under physiological conditions the microbiota shows both: plasticity and high resilience. Upon short-term perturbations (e.g. temporal change in dietary-pattern) the microbial composition adapts to alterations in the intestinal milieu, though soon resembles a pre-disturbance state.7 The microbial ecosystem can also be changed without pathologic consequences for the host and stabilize within a new “alternative state”.35 Animal studies showed that the microbiota is capable to adapt to exposomal factors including diet, antibiotics or intrinsic factors like host genetics. Nevertheless, diet seems to overwrite the influence of genetic imprints.36, 37Rapid resilience to perturbations is a key requirement for intestinal homeostasis in order to maintain a health-associated composition of the ecosystem (“eubiosis”). However, this resilience is lost in some pathologic conditions, like IBD. It is important to note that dysbiosis displays several features, which will be categorized below in i) reduced bacterial diversity, ii) expansion of pathobionts, iii) changes in the microbial composition and iv) change in microbial functional capacity. The appearance of these characteristics may occur solitarily, successively or simultaneously (Figure 2). Upon short term perturbations the microbiota may shift in diversity, composition and function and stabilize again in its previous state, or an alternative state due to high resilience. However, in IBD the microbiota shows low resilience and is subjected to changes finally leading to dysbiosis. The widely discussed attribute of dysbiosis is reduced bacterial diversity. Based on numbers of bacterial species and their abundance found within one sample, the alpha diversity can be calculated. Many studies associated lowered bacterial diversity to disease, with the rationale of loss in metabolic redundancy.32, 38-41 Furthermore, the ability to outcompete pathogens by a low-diverse microbiota is diminished. In patients that underwent frequent antibiotic treatments, the deteriorated intestinal diversity was shown to increase the risk of infection by opportunistic pathogens, such as Clostridium difficile.42 In animal models, pathogens including Salmonella, Citrobacter rodentium or enterohaemorrhagic E. coli (EHEC) fail to colonize in the presence of a diverse, undisturbed microbiota, but elicit pathogenic traits if competing strains are missing.43-46 The mechanisms of competitive exclusion may correspond to rivalry for nutrients or virulence-modulation of intruding strains.47