Campylobacter jejuni genotypes associated with post-infection irritable bowel syndrome

<i>Campylobacter</i> enterocolitis can lead to post-infection irritable bowel syndrome (PI-IBS) but the factors promoting its emergence are poorly understood. While some <i>C. jejuni</i> strains are more significant for human disease, genomic and virulence characteristics that promote PI-IBS development are unknown. We combined pangenome-wide association studies and laboratory microbiology to compare <i>C. jejuni </i>from patients that develop PI-IBS with those that do not. Variation in bacterial stress response (<i>Cj0145_phoX</i>), adhesion protein (<i>Cj0628_CapA</i>), and core biosynthetic pathway genes (biotin: <i>Cj0308_bioD</i>; purine: <i>Cj0514_purQ</i>; isoprenoid: <i>Cj0894c_ispH</i>) associated with PI-IBS development. <i>In vitro </i>assays demonstrated enhanced adhesion, invasion, epithelial barrier disruption, and IL-8 secretion with PI-IBS strains. Twenty-two genomic markers, four of which in an uncharacterized gene <i>Cj1631c, </i>were used to develop a risk-score for PI-IBS development. Demonstrating that specific <i>Campylobacter</i> genotypes confer greater <i>in vitro</i> virulence and increased risk of PI-IBS has potential to improve understanding of the complex host-pathogen interactions underlying this condition.