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.

Comparative Analysis of Peptidoglycans From Pseudomonas aeruginosa Isolates Recovered From Chronic and Acute Infections

“…This pioneer work reveals a perhaps unexpected high degree of stability in the peptidoglycan-related features in very diverse clinical strains of P. aeruginosa , including those highly adapted to the particular environment of the CF airway. In contrast with previous works defending that adaptation to CF could include the selection of changes driving to reduced inflammatory capacity of the peptidoglycan (Cigana et al, 2009, 2011), or several studies in other gram negative species showing that cell wall can accumulate adaptations to better resist within the host (Rosenthal et al, 1982; Swim et al, 1983; Costa et al, 1999; Dillard and Hackett, 2005; Chaput et al, 2006; Humann and Lenz, 2009; Wang et al, 2009, 2010, 2012; Davis and Weiser, 2011; Sukhithasri et al, 2013; Hernández et al, 2015; Frirdich et al, 2019; Schaub and Dillard, 2019a, b), our results with extensive collections of P. aeruginosa suggest that its peptidoglycan is conserved to a higher extent (even including comparisons between exponential and stationary growth phases), and probably, less susceptible of accumulating adaptive changes. Nevertheless, these results do not ensure that if analyzing the peptidoglycans of our strains grown in conditions mimicking their originative host features (i.e., presence of antibiotics, immune compounds, and mainly biofilm growth in CF), the same overall stability would have been observed.…”

Building peptidoglycan inside eukaryotic cells: A view from symbiotic and pathogenic bacteria

“…Such activity could minimize release of PG fragments bearing this motif known as potent NOD1 inducers. Analogous activities decreasing the relative levels of stem peptides bearing immunostimulatory motifs have been described in Helicobacter pylori (Costa et al, 1999) and Campylobacter jejuni (Frirdich et al, 2019). These two pathogens undergo transition to a coccoid morphology concomitant to an increase in muropeptides with short dipeptide side chains at expenses of those having tri-and tetrapeptides.…”

“…These two pathogens undergo transition to a coccoid morphology concomitant to an increase in muropeptides with short dipeptide side chains at expenses of those having tri‐ and tetrapeptides. For both pathogens, the coccoid morphology is achieved following action of dedicated amidases and endopeptidases resulting in a PG with reduced capacity to activate NOD1 (Chaput et al, ; Frirdich et al, ). Intracellular Legionella pneumophila also encodes a periplasmic protein, EnhC, which impairs activity of the PG glycosidase Slt to minimize release of immunostimulatory PG fragments (Liu et al, ).…”

Review on Stress Tolerance in Campylobacter jejuni

“…Campylobacter does not usually grow in environments of atmospheric oxygen (air) due to it being microaerophilic and requiring 5–10% carbon dioxide (CO 2 ) ( Frirdich et al, 2019 ). Campylobacter can tolerate oxidative stress even after exposure towards aerobic conditions ( Kim et al, 2015 ).…”