Might we one day see new ways to diagnose and manage celiac disease (CD)? An article published in September in CLN probes just that question, taking an in-depth look at where research stands on an illness for which scientists thought they had all the answers. “Evidence shows that CD, an intestinal inflammatory disease, occurs in genetically susceptible individuals once they are exposed to proteins like gliadin, secalin, and hordein found in wheat and other grains,” writes senior editor Genna Rollins. And while this still holds true for the autoimmune disorder, “a confluence of basic science discoveries and natural history and observational studies is providing a more nuanced picture of CD,” according to CLN.

Research has determined that the gut microbiome is a player in turning genetic predisposition and environmental exposure into a full-blown autoimmune response, and further studies are underway. Also, the National Institutes of Health’s Human Microbiome Project and next-generation sequencing technologies have provided data and methods to look more seriously at gut microflora’s role in CD.

For example, one 2012 proof-of-concept study showed 2-year longitudinal changes in the intestinal microbiota of babies genetically at risk for CD. The team characterized the gastrointestinal colonization process using pyrosequencing, a quantitative polymerase chain reaction assay, and 1H-nuclear magnetic resonance spectroscopy. The researchers found that genetically susceptible babies first exposed to gluten at age 1 year, rather than between 6 to 8 months, showed a decreased immune response to gluten. They also found a dearth of phylum Bacteroidetes in these infants, a finding that stood in contrast to other studies.

That 2012 study and other research have led to an international study that aims to enroll 500 infants with the goal of identifying and validating a specific microbiotic and metabolomics profile that predicts loss of tolerance to gluten and development of CD, CLN reports. Eventual findings from this investigation could lead to better diagnostics and treatments not only for CD but also for other autoimmune diseases, writes Rollins.