The Production of Listeriolysin O and Subsequent Intracellular Infections by Listeria monocytogenes Are Regulated by Exogenous Short Chain Fatty Acid Mixtures

• Published in: Toxins Vol. 12; no. 4; p. 218
• Main Authors: Rinehart, Erica, Chapman, Julia, Sun, Yvonne
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 30-03-2020; MDPI
• Subjects: aerobic; anaerobic; Animals; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Bacterial Toxins - genetics; Bacterial Toxins - metabolism; Caco-2 Cells; Carbohydrates; Exposure; Fatty acids; Fatty Acids, Volatile - pharmacology; Fibroblasts; Foodborne pathogens; Gene expression; Gene Expression Regulation, Bacterial; Heat-Shock Proteins - genetics; Heat-Shock Proteins - metabolism; Hemolysin Proteins - genetics; Hemolysin Proteins - metabolism; hly; Hly gene; Humans; Infections; Intestine; Intracellular; Levels; Listeria; Listeria monocytogenes; Listeria monocytogenes - drug effects; Listeria monocytogenes - genetics; Listeria monocytogenes - metabolism; Listeria monocytogenes - pathogenicity; Listeriolysin O; LLO; Mice; Mutants; Mutation; Oxygen; Oxygen - metabolism; Oxygen enrichment; Pathogenesis; Peptide Termination Factors - genetics; Peptide Termination Factors - metabolism; Physical fitness; Pore formation; Post-transcription; RAW 264.7 Cells; short chain fatty acids; Sigma Factor - genetics; Sigma Factor - metabolism; Toxins; Transcription, Genetic; Virulence; Listeria monocytogenes; anaerobic; aerobic; hly; LLO; short chain fatty acids
• ISSN: 2072-6651; 2072-6651
• DOI: 10.3390/toxins12040218

is a foodborne pathogen capable of secreting listeriolysin O (LLO), a pore-forming toxin encoded by the
gene. While the functions of LLO have been studied extensively, how the production of LLO is modulated by the intestinal environment, devoid of oxygen and enriched in short chain fatty acids (SCFAs), is not completely understood. Using
strain 10403s, we found that
transcription was moderately decreased by aerobic SCFA exposures but significantly increased by anaerobic SCFA exposures. Moreover, aerobic, but not anaerobic, exposure to low levels of SCFAs resulted in a significantly higher LLO activity. These results demonstrated that transcriptional and post-transcriptional regulations of LLO production were separately modulated by SCFAs and were responsive to oxygen levels. Examining isogenic mutants revealed that PrfA and SigB play a role in regulating LLO production in response to SCFAs. Effects of SCFAs were also present in the cardiotropic strain 07PF0776 but distinctly different from those in strain 10403s. For both strains, prior exposures to SCFAs altered intracellular infections in Caco-2 and RAW264.7 cells and the plaque sizes in L fibroblasts, a result confirming the ability of
to adapt to SCFAs in ways that impact its subsequent infection outcomes.