There is also good evidence of probiotic modulation of DCs towards a proregulatory function [15,28]. Of course, not all commensals are down-regulatory, and some (like Helicobacter hepaticus) may be pathogenic in some settings, yet induce Tregs in others [29]. Furthermore, there can be significant interactions between pathogens, as in the example of intestinal bacteria aggravating the immunopathology caused by Toxoplasma infection [30]. In the latter setting, there is reduced floral complexity, either because of relative loss of more ‘regulatory’ strains or simply as a broad reflection of an altered selleck inhibitor homeostasis accompanying

pathogenesis. One consequence of the immune system’s reliance on microflora for optimal immunoregulation is that antibiotic therapies may result in unintended activation of immune effector mechanisms. In model systems, antibiotic treatment renders mice more susceptible to induction of food allergy [7] as well as allergic airway inflammation [31]. For the human population, antibiotics are seen as major modifiers of beneficial human–microbe interactions [32] learn more superimposed upon alterations caused by other exogenous factors including urbanization, global travel and dietary changes [33]. The acute effects of antibiotic treatment on the native gut

microbiota range from self-limiting diarrhoea to life-threatening pseudomembranous colitis induced by bacteria filling the niche provided by the reduction in bacterial diversity [34]. The long-term consequences of such perturbations for the human–microbial symbiosis are more difficult to discern, but chronic conditions such as asthma and atopic disease have been associated with childhood antibiotic use Tolmetin and an altered intestinal microbiota [35–37]. Because many chemical

transformations in the gut are mediated by specific microbial populations, with implications for, among others, cancer and obesity, changes in the composition of the gut microbiota could have important but undiscovered health effects. In this regard, ciprofloxacin treatment of healthy volunteers influenced the abundance of about a third of the bacterial taxa in the gut, decreasing the taxonomic richness, diversity and evenness of the community. However, the magnitude of this effect varied among individuals, and some taxa showed interindividual variation in the response to ciprofloxacin. In each individual, the taxonomic composition of the community closely resembled its pretreatment state by 4 weeks after the end of treatment, but several taxa failed to recover within 6 months [38]. The production of active anti-inflammatory mediators by particular commensal species (reviewed in [39]) provides a mechanistic framework for microbial regulation of pathology in the GI tract.