Project description:Listeria monocytogenes is the ubiquitous food-borne pathogen which causes listeriosis, a disease with a high mortality rate, mostly transmitted through contaminated ready-to-eat foods (EFSA, 2018). To better understand the systemic response of such microorganism exposed at three environmental factors (T, pH and NaCl), the proteome of a L. monocytogenes strain, which was isolated from a meat product (Coppa di testa) linked to a listeriosis outbreak occurred in Marche region (Italy) in 2016, was investigated in order to identify differences in its protein patterns.
Project description:Transcriptional profling of a Listeria monocytogenes under nisin treatment comparing ctsR mutant and wild type one condition (nisin treament 20ug/ml, 24 hours) experiment, ctsR mutant vs. wild type Listeria monocytogenes Scott A, 2 biological replicates, 4 technical replicates
Project description:Listeria monocytogenes is a common clinical pathogen primarily transmitted among humans and animals through contaminated food. Currently, the increasing prevalence of antibiotic resistance due to the misuse of antibiotics has become a significant problem, leaving both clinical medicine and agriculture with a lack of effective treatments for Listeria infections. Listeriolysin O (LLO), a virulence factor secreted by Listeria monocytogenes, is a key factor in its pathogenicity. Strains of Listeria monocytogenes lacking the LLO gene are non-pathogenic to humans and animals. Therefore, studying the molecular mechanisms of LLO degradation is of great practical significance for treating clinical infections caused by antibiotic-resistant Listeria. Additionally, it will provide a theoretical basis for developing new antimicrobial drugs. Since Listeria monocytogenes secretes LLO throughout its entire life cycle within the host cell, understanding the fate of LLO at different stages of infection is crucial for elucidating the pathogenic mechanisms of Listeria monocytogenes. It is already known that LLO secreted by Listeria within the phagosome can be degraded via the lysosomal pathway. However, the fate of LLO secreted by Listeria in the cytoplasm remains poorly understood. Based on our previous experimental data and relevant literature, we propose a novel hypothesis that the AP-2 complex targets and degrades LLO secreted by Listeria in the cytoplasm.
Project description:This study will evaluate the safety and tolerability of a personalized live, attenuated, double-deleted Listeria monocytogenes (pLADD) treatment in adults with metastatic colorectal cancer.
Project description:Investigation of whole genome gene expression level changes in Listeria monocytogenes LO28 delta-lhrC1-5 mutant, compared to the wild type strain. The lhrC1-5 genes encode the regulatory sRNAs LhrC1-5. The microarray studied the gene expression of unstressed cells and cells exposed to cefuroxime for 30 min. The lhrC1-5 mutant employed in this study is further described in Sievers et al. (2014) A multicopy sRNA of Listeria monocytogenes regulates expression of the virulence adhesin LapB. Nucleic Acids Res. 42:9383-98.
Project description:Comparison of Listeria monocytogenes transcripts in different strains (EGD wild-type versus EGD-e wild-type, EGD-e PrfA* versus EGD-e wild-type).
Project description:Comparison of Listeria monocytogenes transcripts in different strains (EGD wild-type versus EGD-e wild-type, EGD-e PrfA* versus EGD-e wild-type).
Project description:The formation of Listeria monocytogenes biofilms contributes to persistent contamination in food processing facilities. A microarray comparison of L. monocytogenes between the transcriptome of the strong biofilm forming strain (Bfms) Scott A and the weak biofilm forming (Bfmw) strain F2365 was conducted to identify genes potentially involved in biofilm formation. Among 951 genes with significant difference in expression between the two strains, a GntR-family response regulator encoding gene (LMOf2365_0414), designated lbrA, was found to be highly expressed in Scott A relative to F2365. A Scott A lbrA-deletion mutant, designated AW3, formed biofilm to a much lesser extent as compared to the parent strain by a rapid attachment assay and scanning electron microscopy. Complementation with lbrA from Scott A restored the Bfms phenotype in the AW3 derivative. A second microarray assessment using the lbrA deletion mutant AW3 and the wild type Scott A revealed a total of 304 genes with expression significantly different between the two strains, indicating the potential regulatory role of LbrA in L. monocytogenes. A cloned copy of Scott A lbrA was unable to confer enhanced biofilm forming potential in F2365, suggesting that additional factors contributed to weak biofilm formation by F2365. Findings from the study may lead to new strategies to modulate biofilm formation. Two comparisons were performed between 1) strong biofilm former Listeria monocytogenes strain ScottA versus weak biofilm former Listeria monocytogenes strain F2365; 2) Listeria monocytogenes ScottA LbrA deletion mutant strain versus Listeria monocytogenes ScottA. Four replicates were loaded for the first comparison and two replicates were loaded for the second comparison.
