Infections by Campylobacter species are the most common foodborne
zoonotic disease worldwide. Campylobacter jejuni and C. coli are isolated most frequently from human stool samples, but severe
infections by C. fetus (Cf), which can cause
gastroenteritis,
septicemia, and abortion, are also found. This study aims at the characterization of pathological changes in Cf
infection using an intestinal epithelial cell model. The Cf-induced epithelial barrier defects appeared earlier than those of avian Campylobacter species like C. jejuni/C. coli. Two-path impedance spectroscopy (2PI) distinguished transcellular and paracellular resistance contributions to the overall epithelial barrier impairment. Both transcellular and paracellular resistance of Cf-infected HT-29/B6 monolayers were reduced. The latter was attributed to activation of active
anion secretion. Western blot analysis showed no decrease in tight junction (TJ)
protein expression (claudin-1, -2, -3, and -4) but showed redistribution of
claudin-1 off the TJ domain. In addition, Cf induced epithelial cell death, cell detachment, and lesions (focal leaks), as the result of which macromolecule flux (10-kDa dextran) was increased in Cf-invaded cell monolayers. In conclusion, barrier dysfunction from Cf
infection was due to TJ
protein redistribution, cell death induction, and leak formation, resulting in bacterial translocation, ion leak flux, and
antigen uptake (leaky gut).