The Campylobacter jejuni helical to coccoid transition involves changes to peptidoglycan and the ability to elicit an immune response.

Abstract

Summary Campylobacter jejuni is a prevalent enteric pathogen that changes morphology from helical to coccoid under unfavorable conditions. Bacterial peptidoglycan maintains cell shape. As C. jejuni transformed from helical to coccoid, peptidoglycan dipeptides increased and tri‐ and tetrapeptides decreased. The DL‐carboxypeptidase Pgp1 important for C. jejuni helical morphology and putative N‐acetylmuramoyl‐L‐alanyl amidase AmiA were both involved in the coccoid transition. Mutants in pgp1 and amiA showed reduced coccoid formation, with ∆pgp1∆amiA producing minimal coccoids. Both ∆amiA and ∆amiA∆pgp1 lacked flagella and formed unseparated chains of cells consistent with a role for AmiA in cell separation. All strains accumulated peptidoglycan dipeptides over time, but only strains capable of becoming coccoid displayed tripeptide changes. C. jejuni helical shape and corresponding peptidoglycan structure are important for pathogenesis‐related attributes. Concomitantly, changing to a coccoid morphology resulted in differences in pathogenic properties; coccoid C. jejuni were non‐motile and non‐infectious, with minimal adherence and invasion of epithelial cells and an inability to stimulate IL‐8. Coccoid peptidoglycan exhibited reduced activation of innate immune receptors Nod1 and Nod2 versus helical peptidoglycan. C. jejuni also transitioned to coccoid within epithelial cells, so the inability of the immune system to detect coccoid C. jejuni may be significant in its pathogenesis.