Prevalence of Premature Stop Codons (PMSCs) in Listeria monocytogenes isolated from clinical and food samples in Iran

Abstract

BackgroundListeria monocytogenes utilizes internalin A (InlA; encoded by inlA) and facilitates the entrance to non-phagocytic cells with E-cadherin expression. Several naturally occurring point mutations leading to a premature stop codon (PMSC) in inlA have been reported, which are known to produce truncated proteins. This study aimed to determine the prevalence of PMSCs in L. monocytogenes isolated from clinical and food samples in Iran. MethodsIn this study, a total of 50 L. monocytogenes isolates were obtained from the microbial bank of the microbiology department of Iran University of Medical Sciences, Tehran, Iran. These samples consisted of 27 clinical samples and 23 food samples. DNA extraction was carried out after culture, isolation and biochemical confirmation of the isolates. Then, inlA gene was sequenced in order to identify PMSCs mutation. ResultsThe results of our study showed that 16.6% of food isolates and 1.4% of clinical isolates possessed inlA gene with PMSC mutation. Mutation in food isolates resulted in a shorter sequence of inlA gene compared with the mutation in clinical isolates. It is possible that the truncated proteins caused by PMSCs are able to attach the surface receptors on epithelial cells. Therefore, it is important to know the exact location in which PMSCs occur. ConclusionResults showed that mutations causing PMSCs in inlA gene are more common in food isolates rather than clinical isolates.