The or plant-based diet for a short period

The first factor influencing the acquisition of microbes is the mode of delivery. Also early nutrition (breast- or formula-feeding) or hygienic environment (lifestyle and geographic location) in which a child is raised determines the composition of microorganisms. In later life, the sum of environmental triggers, the so-called exposome, including e.g. diet, stress, hygienic milieu (contact to disinfectants or animals), drugs and geography (e.g. air pollution) contribute to shape the intestinal ecosystem.3, 41, 71-79 The daily diet has an enormous impact on the intestinal ecosystem. Especially diet high in fat seems to shift the microbiota towards a more dysbiotic pattern, which is associated with increased risk of intestinal inflammation. Animal, as well as human studies showed the rapid adaption to changed dietary patterns. By feeding mice an exclusively animal- or plant-based diet for a short period of time, David et al. effectively showed the plasticity, as well as the stability of the intestinal ecosystem upon short-term perturbations.80 However, also other studies showed that clear shifts in the intestinal ecosystem diversity and composition are not induced by short term changes in dietary habits or application of single nutrients, but require long term pressure on the ecosystem.7, 81 Beside exposomal factors, also intrinsic factors i.e. the respective genetic structure of the host, shape the intestinal microbiota. Several genes associated with altered immune function, microbial recognition or antimicrobial defence were shown to influence the intestinal ecosystem. In a meta-analysis Knights et al. highlighted the significant association between the NOD2 risk allele and increased abundance of Enterobacteriaceae in IBD patients.82 In another study, Rausch et al. showed an association between the intestinal microbiota and the fucosyltransferase 2 (FUT2) secretor gene – a physiological trait that regulates gastrointestinal mucosal expression of blood group A and B antigens. Approximately 20% of humans lack the FUT2 gene, which was shown to be a risk factor for CD development.83 Within the group of CD patients, the microbiota from FUT2 carriers differed from non-secretors in composition, diversity and metabolic functionality.84, 85This observation of dysbiosis before onset of pathologies is exceptionally interesting, as recent studies also suggest that inflammatory conditions directly influence the intestinal community. This shift may occur due to insufficient bacterial adaptation to the changed milieu found during inflammatory processes. During inflammation, the secretion of antimicrobial peptides (AMPs) is upregulated. A recent study reported that the colonization fitness of commensals depends on the capability to adjust to increased AMP levels.86 Therefore, some community members will be displaced during inflammation. While pathogens or pathobionts cannot survive these increased AMP levels, commensals are resistant. In this manner, stability and resilience during infections is mediated. The potential of AMPs to shape the intestinal ecosystem and their importance in IBD has been shown by others before.87 The inflammatory reactions may also induce stress or upregulation of virulence-associated genes in the microorganism, as shown in monoassociation-studies with the gut commensals Enterococcus faecalis OG1RF or E. coli NC101.88, 89 E. coli NC101 cells isolated from inflamed IL-10-/- mice displayed upregulated bacterial-stress response genes (e.g. heat shock proteins) compared to isolates from WT mice.89, 90 However, inflammation may also promote growth-advantages and virulence of pathogens. For Salmonella typhimurium (S. typhimurium) it was shown that the host produces tetrathionate under inflammatory circumstances. This subsequently promotes the ethanolamine-utilization of S. typhimurium and thereby its colonization fitness.91, 92 Also nitrate, which is produced by the host during inflammation, is assumed to promote growth of Enterobacteriaceae. Consequently, the often discussed increase of Enterobacteriaceae in IBD may also be regarded as secondary event to inflammatory processes rather than a causative association.58