By Teresa Conrick
A newer study caught my eye very recently, Distinct Microbiome-Neuroimmune Signatures Correlate With Functional Abdominal Pain in Children With Autism Spectrum Disorder . It´s a very interesting and important paper as the authors describe - The ability to pinpoint key differences in the mucosal microbiome of these children was in part owing to improvements in technology. Improved sequencing technology and deeper sequencing, particularly in a low-biomass sample such as tissue, enabled the data to be better classified. That is NEW.
Why that´s important is huge as we are able to see that there are specific TYPES of bacteria causing havoc and PAIN for too many children. If we know the enemy, the hope is to stop that pain and improve functioning for that person. Here is their summary (FGID stands for functional gastrointestinal disorders):
In summary, GI phenotypes in ASD are highly variable, and heterogeneity of the autism population can mask significant signals related to GI symptomology. Here, we present distinct microbiome and cytokine measures in the rectal mucosa of children with ASD and confirmed FGIDs compared with neurotypical children both with and without FGIDs. From rectal biopsy specimens obtained during endoscopy, deep molecular analysis of the mucosal microbiome in ASD-FGID showed distinct microbial communities at the predicted species level. Correlations of Clostridiales, including multiple Clostridium species previously associated with ASD, with tryptophan, serotonin, and inflammatory cytokine levels yielded a unique multi-omic profile specific to ASD-FGID and ASD-FGID with abdominal pain. Cytokines indicative of inflammation correlated strongly with several bacteria associated with ASD-FGID, as was the case with tryptophan levels, and these potential associations will be confirmed in future work. These data suggest the presence of a specific microbiome profile in ASD with the identification of organisms previously strongly associated within similar cohorts, albeit in stool-based studies. We advance this concept by showing that these ASD-related organisms interact with the intestinal mucosa and are associated with altered neuroimmune signaling. Although these initial findings are correlative, these data form the framework for future studies targeting tryptophan–serotonin metabolism and inflammatory pathways in FGID in ASD.