Objective Previous studies of AN showed low‐grade inflammation. Are low‐grade inflammation and circulating lymphocytes associated with chronic conditions? Method Peripheric blood cytokines were measured using Luminex™ technology in a chronic AN cohort (mean = 67.42 months), compared to Constitutional Thinness (CT), Constitutional Obesity (CO), and Healthy Controls (HC). Secondarily a prospective cohort of chronic AN (mean = 54.11 months) was recruited to compare the functional lymphocyte profile in blood by flow cytometry to CT and HC. Results In the AN group, most cytokine concentrations were lower than in CT and HC groups. The IL‐23 (98.02 pg/ml) was elevated related to HC and CO, and the IL‐10 (4.178 pg/ml) was elevated versus CO. In the CT group, IL‐9 (0.06216 pg/ml) was elevated compared to AN. The AN group had high Treg (9.259% of CD4+) and CD8+Integrinβ7+ (9.552% of CD3+) versus HC for lymphocyte populations. In CT group, elevated Treg (9.7% of CD4+) elevated percentage of CD4+CCR9+ (5.867% of CD3+) and CD8+Integrinβ7+ (10.21% of CD3+) were found versus HC. Conclusions The chronic state of AN and CT is surprisingly non‐inflammatory with elevated Treg cells. These results suggest that maintaining a dysregulated response to intestinal antigens may contribute to maintaining AN.

Mental health is becoming a public health priority worldwide. Anorexia nervosa and autism spectrum disorders are 2 important types of childhood disorders with a bad prognosis. They share cognitive impairments and, in both cases, the microbiota appears to be a crucial factor. Alteration of the microbiota-gut-brain axis is an appealing hypothesis to define new pathophysiological mechanisms. Mucosal immunity plays a key role between the microbiota and the brain. The mucosal immune system receives and integrates messages from the intestinal microenvironment and the microbiota and then transmits the information to the nervous system. Abnormalities in this sensorial system may be involved in the natural history of mental diseases and might play a role in their maintenance. This review aims to highlight data about the relationship between intestinal mucosal immunity and these disorders. We show that shared cognitive impairments could be found in these 2 disorders, which both present dysbiosis. This literature review provides details on the immune status of anorexic and autistic patients, with a focus on intestinal mucosal factors. Finally, we suggest future research hypotheses that seem important for understanding the implication of the gut-brain-axis in psychiatric diseases.

Inflammatory bowel diseases (IBD) are complex chronic inflammatory disorders of the gastrointestinal (GI) tract. Recent evidence suggests that the gut-brain axis may be pivotal in gastrointestinal and neurological diseases, especially IBD. Here, we present the first proof of concept for a microfluidic technology to model bilateral neuro-immunological communication. We designed a device composed of three compartments with an asymmetric channel that allows the isolation of soma and neurites thanks to microchannels and creates an in vitro synaptic compartment. Human-induced pluripotent stem cell-derived cortical glutamatergic neurons were maintained in soma compartments for up to 21 days. We performed a localized addition of dendritic cells (MoDCs) to either the soma or synaptic compartment. The microfluidic device was coupled with microelectrode arrays (MEAs) to assess the impact on the electrophysiological activity of neurons while adding dendritic cells. Our data highlight that an electrophysiologic signal is transmitted between two compartments of glutamatergic neurons linked by synapses in a bottom-up way when soma is exposed to primed dendritic cells. In conclusion, our study authenticates communication between dendritic cells and neurons in inflammatory conditions such as IBD. This platform opens the way to complexification with gut components to reach a device for pharmacological compound screening by blocking the gut-brain axis at a mucosal level and may help patients.