#19 Irritable Bowel Syndrome-Related Neurotransmitters Transporters and Metabolism Gene Expression but Not Gut Microbiota are altered in a Rat Model of Post-Traumatic Stress Disorder
Omar Elgazzar, University of Manitoba; Nour Eissa, University of Manitoba; Laëtitia Kermarrec, University of Manitoba; Gilbert Kirouac, University of Manitoba; Jean-Eric Ghia, University of Manitoba
Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by abdominal discomfort, gut microbiota dysbalance and affecting 5 million Canadians. Post-traumatic-stress disorder (PTSD) is the experience of a physical or emotional event involving intense fear leads to a strong emotional reaction. As PTSD has been identified as a potential contributing factor for the development of IBS, we hypothesized that PTSD may promote the disease. Aim: The aims of this study were to determine whether a PTSD could (1) alter the IBS-associated genes; (2) or the gut microbiota.
PTSD-model: Male rats were handled every second day for a total of 4 times before shock procedure to be given on day 1. Rats were given foot-shocks (5 × 2 s of 1.5 mA presented randomly over 2 min with an inter-shock period of 10-50 s). Non-shock rats have been placed in the chamber for the same amount of time. On day 14, all behavioral tests have been videotaped and analyzed. Sampling: Colon samples were collected from shocked and control groups then subjected to IBS-related gene expression analysis. Feces and mucosa associated microbiota (MAM) samples were collected, and the V4 region of 16s rRNA was subjected to Miseq-Illumina sequencing.
PTSD resulted in a decrease in colonic gene expression of neurotransmitter transporters (neuropeptide S receptor-1 (Npsr1), serotonin transporter (Sert)), and an increase in neurotransmitter metabolism markers (sodium voltage gated channel alpha subunit 5 (Scn5a), fatty acid amide hydrolase (Faah)). Conversely, the inflammatory markers (Tumor necrosis factor-(Tnf)a, Interleukin-(Il)-10, Toll-like receptor (Tlr)9 and receptors (Adrenoceptor-Alpha-2C (Adra2c), Koltho-Beta (Klb), KDEL-Receptor-2 (Kdelr2)) did not show any changes. PTSD did not show a significant effect at the phylum or genus levels in both fecal and MAM.
PTSD can contribute to the pathogenesis of IBS through alteration of the neurotransmitters transporters/metabolism genes without modifying inflammatory mediators or gut microbiota.