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Abstract
Listeria monocytogenes is a foodborne pathogen capable of secreting listeriolysin O (LLO), a pore-forming toxin encoded by the hly 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 L. monocytogenes strain 10403s, we found that hly 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 L. monocytogenes to adapt to SCFAs in ways that impact its subsequent infection outcomes.
Highlights
Listeria monocytogenes is a Gram-positive, facultative anaerobe and a foodborne pathogen
Supplementations with Mlo short chain fatty acids (SCFAs) resulted in a significant increase in listeriolysin O (LLO) activity while supplementations with Mhi SCFAs resulted in a compromised LLO activity (Figure 2E)
LLO activity in anaerobically grown cultures was too low to calculate hemolytic activity, we showed the results in a dilution curve and noted an elevated LLO activity in cultures supplemented with Mhi SCFAs (Figure 2F)
Summary
Listeria monocytogenes is a Gram-positive, facultative anaerobe and a foodborne pathogen. 1600 people annually are estimated to become infected with L. monocytogenes and hospitalized in the United States, among which as many as one in five patients do not survive, making L. monocytogenes infections contributing to 19% of the overall deaths related to foodborne pathogens [1]. Transmission and infection of L. monocytogenes rely on multiple virulence genes contributing to various stages of pathogenesis—surviving and colonizing the host gastrointestinal tract, binding to and entering host cells, growing inside the host cell cytosol, and spreading from one host cell to another. Transcription of the hly gene, which encodes listeriolysin O (LLO)—a cholesterol-dependent pore forming toxin that facilitates L. monocytogenes entry into the host cell cytosol [3], is responsive to a multitude of environmental factors, ranging from salt concentrations [4], growth temperature [5], to culture pH [5,6]. We have shown that anaerobic conditions and propionate, two important environmental signals present in the intestinal lumen, can impact LLO production [7,8,9]
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