Effect of acid-adaptation onListeria monocytogenessurvival and translocation in a murine intragastric infection model

Abstract

Acid tolerance response mechanisms can greatly influence Listeria monocytogenes survival in low pH foods. In the present paper, the effect of acid-adaptation together with control of gastric pH level on L. monocytogenes survival and translocation was analyzed after intragastric inoculation in the BALB/c mouse model. Our results showed that acid-adaptation led to an increase in resistance to the first barrier constituted by the low gastric pH and that inoculation at alkaline pH had a synergistic effect. It resulted in a higher live bacterial load reaching the next intestinal compartments and was correlated with increased translocation rates to the mesenteric lymph nodes, both at the frequency and quantitative levels. Our results in this murine model suggest that acid-adaptation of L. monocytogenes in low pH foods, together with control of gastric pH level through dietary practices, or use of inhibitors of gastric acid secretion, may be potential aggravating risk factors to food-borne listeriosis.

CD8+T cell priming in oral mucosa-draining lymph nodes supports systemic immunity

“…1F ). This is in line with the notion that > 90% of ingested bacteria are killed by gastric acids (Saklani-Jusforgues et al, 2000; Pitts and D’Orazio, 2018). Residual Lm in the intestinal lumen may have been degraded by digestive enzymes, or failed to cross the mucus layer of the intestinal epithelium or their tight junctions, or become cleared by peristaltic contraction and mucus secretion.…”

Acid shock of Listeria monocytogenes at low environmental temperatures induces prfA, epithelial cell invasion, and lethality towards Caenorhabditis elegans

“…As a result of this acid adaptation process, virulence gene expression probably decreases in L. monocytogenes . Due to the ATR, the acid adapted listeriae also show an enhanced capacity to survive the gastric barrier as reflected by higher survival rates 15 min after intragastric infection of mice [73]. In this case, a further signal for virulence gene induction occurs after stomach exit, namely exposure to short chain fatty acids accompanied with pH neutralization [74].…”

Multifaceted Defense against Listeria monocytogenes in the Gastro-Intestinal Lumen

“…Importantly, L. monocytogenes undergoes a “stress hardening” response in that exposure to moderately low pH (~5.5) increases its resistance to otherwise lethal pH (~3.5) [ 34 ]. This process was shown to increase viability of the pathogen in vivo after oral inoculation, including favoring spread of live bacteria to the mesenteric lymph nodes [ 40 ]. Resistance against low pH in the stomach and duodenum is achieved by L. monocytogenes through several mechanisms, including import and decarboxylation of glutamate and catabolism of arginine to ornithine, both resulting in consumption of protons and increases in intracellular pH [ 41 , 42 , 43 ].…”