Experimental analysis shows short-chain fatty acids reduce growth and virulence in Arcobacter butzleri, implying alterations in pathogen-host interactions.
Aims Arcobacter butzleri, a widespread bacterium linked to gastrointestinal disease, can bypass host colonization resistance mechanisms; however, its response to short-chain fatty acids (SCFAs) remains poorly understood. This study investigated the impact of SCFAs on A. butzleri’s survival and virulence. Methods and Results Eight A. butzleri isolates were assessed under varying concentrations of individual SCFAs and mixtures (m-SCFAs). Higher SCFAs concentrations inhibited bacterial growth in a strain-dependent manner. Transcript analysis of putative virulence genes revealed upregulation of ciaB and flaA across most m-SCFAs concentrations, while luxS expression increased at 90 mM. SCFAs generally reduced bacterial motility, with sodium propionate reducing motility but enhancing biofilm-forming ability in the model strain. Additionally, SCFAs exposure decreased the ability of A. butzleri to adhere to and invade the Caco-2 intestinal epithelial cell line. Whole-genome sequencing of the eight A. butzleri isolates revealed extensive genetic diversity, particularly in virulence- and stress-associated genes, although consistent genotype/phenotype correlations were not observed. Conclusions Altogether, these findings demonstrate that SCFAs modulate A. butzleri survival and virulence, providing novel insights into their significance in shaping pathogen behaviour and host-pathogen interactions.
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