Differential effects of deoxynivalenol and deepoxy–deoxynivalenol on Campylobacter jejuni growth and gene expression

Deoxynivalenol (DON) is the most prevalent trichothecene mycotoxin in poultry feed, and Campylobacter jejuni is a major zoonotic pathogen in broilers. In a recent study, we demonstrated that DON not only increased C. jejuni colonization in the jejunum and cecum of infected birds but also elevated bacterial counts in internal organs. In contrast, its less toxic D metabolite, deepoxy–deoxynivalenol (DOM-1) significantly reduced the Campylobacter levels in vivo. These findings suggest that DON and DOM-1 may exert direct effects on C. jejuni growth dynamics.

The present study aimed to further explore this interaction in vitro through co-incubation and RNA-sequencing. Two C. jejuni strains were investigated: the reference strain NCTC 12744 and a field isolate (strain 1303) obtained from a broiler flock. Both strains (105 CFU/ml) were cultured in 96-well plates and incubated with either DON or DOM-1 (5 and 20 µg/mL) or without additives (as a control), under microaerophilic conditions at 41.5 °C. Bacterial counts were assessed at 6 h intervals from 24 to 48 h (24 h, 30 h, 36 h, 42 h, and 48 h).

Results showed that DON significantly promoted C. jejuni growth beginning at 30 h of incubation. Conversely, DOM-1 markedly reduced C. jejuni CFU counts, confirming the in vivo evidence of its potential to lower C. jejuni colonization in chickens. Additionally, transcriptomic profiling revealed that DON or DOM-1 modulate specific metabolic and regulatory pathways in C. jejuni. In particular, DON exposure upregulated genes related to energy metabolism and stress adaptation, while DOM-1 exposure led to the upregulation of pathways associated with growth inhibition.

These data are the first to demonstrate a direct, opposing influence of DON and its metabolite DOM-1 on C. jejuni growth. Our findings suggest that DON contamination in feed could promote Campylobacter proliferation in poultry, whereas DOM-1 may mitigate it. Understanding these interactions provides novel insights into how feed-derived toxins influence foodborne pathogens and could inform strategies to mitigate Campylobacter risk.