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Campylobacter jejuni genotypes are associated with post-infection irritable bowel syndrome in humans.

Stephanie PetersBen PascoeZuo-Wei WuSion C BaylissXimin ZengAdam EdwinsonSakteesh Veerabadhran-GurunathanSelina JawahirJessica K CallandEvangelos MourkasRobin PatelTerra WiensMarijke DecuirDavid BoxrudKirk SmithCraig T ParkerGianrico FarrugiaQijing ZhangSamuel K SheppardMadhusudan Grover
Published in: Communications biology (2021)
Campylobacter enterocolitis may lead to post-infection irritable bowel syndrome (PI-IBS) and while some C. jejuni strains are more likely than others to cause human disease, genomic and virulence characteristics promoting PI-IBS development remain uncharacterized. We combined pangenome-wide association studies and phenotypic assays to compare C. jejuni isolates from patients who developed PI-IBS with those who did not. We show that variation in bacterial stress response (Cj0145_phoX), adhesion protein (Cj0628_CapA), and core biosynthetic pathway genes (biotin: Cj0308_bioD; purine: Cj0514_purQ; isoprenoid: Cj0894c_ispH) were associated with PI-IBS development. In vitro assays demonstrated greater adhesion, invasion, IL-8 and TNFα secretion on colonocytes with PI-IBS compared to PI-no-IBS strains. A risk-score for PI-IBS development was generated using 22 genomic markers, four of which were from Cj1631c, a putative heme oxidase gene linked to virulence. Our finding that specific Campylobacter genotypes confer greater in vitro virulence and increased risk of PI-IBS has potential to improve understanding of the complex host-pathogen interactions underlying this condition.
Keyphrases
  • irritable bowel syndrome
  • biofilm formation
  • escherichia coli
  • antimicrobial resistance
  • pseudomonas aeruginosa
  • copy number
  • candida albicans
  • rheumatoid arthritis
  • gene expression
  • small molecule
  • preterm infants