Completion Date
6-2019
Advisor(s)
Marie Yeung
Abstract
Over the past decade, interest in the use of probiotics, or “good bacteria”, for human health advancement and remediation has grown. Previous studies have shown that some health benefits conferred by probiotics are strain specific, therefore individual probiotic effects must be evaluated. This study evaluated some probiotic candidates on their ability to produce metabolites which inhibit the growth of foodborne pathogens. Probiotics are known to inhibit growth of other bacteria through competitive exclusion and production of bactericidins. In addition, previous studies have established that some probiotics promote the integrity of tight junctions, proteins that play a role in intestinal epithelial cell adherence and regulation of ion transport between intestinal cells and the lumen. In conclusion, observed growth inhibition varies based on assay method. L. monocytogenes exhibited a 2-4 mm zone of inhibition for probiotic culture via lawn assay and V. cholerae exhibited a 6-8 mm zone of inhibition for probiotic culture and sterile probiotic supernatant via lawn assay. PH adjustment of the probiotic supernatant to ~6.8 decreased its inhibitory effects on both pathogens’ growth and increased pathogen recovery from liquid co-cultures. Therefore, the major growth inhibitory mechanism is likely related to the acidity of probiotic the supernatant. The average TEER of probiotic treated Caco-2 cells is the same or slightly greater than that of untreated Caco-2 cells, indicating that tight junction integrity stays relatively stable with probiotic treatment. Probiotic treatment does not appear to rescue TEER decrease in Caco-2 cells after V. cholerae application. These data bolster a plethora of studies that suggest that probiotic bacteria may indeed be beneficial for human health, through inhibition of pathogenic growth of V. cholerae and L. monocytogenes via secretion of acid; however further work must be done using extensive in vivo models to validate these findings.
URL: https://digitalcommons.calpoly.edu/bkendowments/98
Copyright
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