While much of the evidence to date suggesting a link between the gut microbiota and autoimmune disease comes from differences in pathology between GF and conventionalized mice, there are numerous human association studies to suggest that such findings are applicable to humans [4,14].
In children with new-onset Crohn’s Disease, antibiotics amplified the changes in the microbiota and caused a mild increase in disease severity. 16S sequencing revealed that antibiotics in these children triggered a major reduction in taxa including Bacteroidales and Erysipelotrichaceae, which are typically associated with noninflammatory conditions .
At least nine studies based on questionnaires or database searches have shown an increased likelihood of IBD diagnosis in people who have taken antibiotics . Although these studies have mostly focused on children, there is limited evidence that adults who receive antibiotics have an increased chance of developing IBD within 2–5 years .
Similar database searches have shown that antibiotic use is associated with an increased risk of diabetes, childhood asthma, and a 30% higher risk of MS development [17,18,19]. Though correlative studies such as these cannot prove causation, they provide collateral evidence for the hypothesis that an altered microbiota can contribute to disease, which is well supported by mouse studies.
Antibiotic use early in life has been shown to change the gut microbiota in mice and lead to increased weight gain in both mice and humans [10,20].
Antibiotics also can influence the host directly. A transfer experiment using GF mice showed the increased weight gain in mice was due to microbiota changes, not antibiotic exposure .
Antibiotic use also increases susceptibility to infection . In the case of Clostridium difficile, this can prove fatal. Currently the treatment with the highest cure rate for C. difficile infection, >90% in many trials, is Fecal Microbiota Transplant (FMT) .
Recent discoveries showing the influence of the gut microbiota on stem cells and brain function suggest that the list of disorders associated with an altered early-life gut microbiome will continue to expand [23,24].
Moving beyond database correlations and small clinical trials to determine causal roles in humans is a major challenge facing researchers in the field.