Browsing by Subject "Listeria monocytogenes"

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    An Economic Analysis of Cost Trends in Listeria Monocytogenes Recalls from Meat, 2010 - 2024
    (2025-04) Lachinski, Melia
    Listeria monocytogenes is a strand of bacteria that causes foodborne illness. Recalls tend to be costly through both direct and indirect measures. Previous research has uncovered that loss of human life, illness, and amount of product highly impact the cost of food recalls. Using a model adapted from previous research on the economic cost of food recalls, this paper seeks to find the driving explanatory variables of the total cost of Listeria monocytogenes recalls of meat products. The data sampled was collected from the USDA FSIS’s publications on Listeria monocytogenes recalls from 2010 to 2024. A statistical multiple linear regression was performed to determine the presences of correlation between possible explanatory variables and the response variable at a significance level of 0.05. Of the selected variables, days of delayed communication and pounds of product recalled produced p-values less than the significance level, establishing a relationship between these explanatory variables and the response of cost. This implies that these variables constitute the driving variable most capable of predicting the overall cost of a Listeria monocytogenes recall from meat products.
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    Immune suppressive molecules and regulatory T cells control host defense against listeria monocytogenes infection
    (2012-06) Rowe, Jared Hamilton
    The mammalian immune response is an intricately regulated, dynamic process providing the host with protection from the vast number of pathogenic microorganisms. Herein, these studies identified the impacts of regulating host defense by immune suppressive mechanisms, following infection with the bacterial pathogen Listeria monocytogenes. These investigations identified that changes in the inflammatory signals present during Listeria infection resulted in drastically different outcomes in the priming of protective T cells, when these cells were stimulated by either the immune suppressive molcules Cytotoxic T Lymphocyte Antigen (CTLA)-4 or Program Death Ligand (PDL)-1. Due to these findings, whereby changes in the immunologic environment altered the function of suppressive molecules, we examined whether physiologic changes in the immune system would impact host defense to infection. The natural expansion of the immune suppressive regulatory T cell (Tregs), while essential for sustaining pregnancy, resulted in increased maternal susceptibility to Listeria infection. Morevoer, Listeria entry into the host cell cytoplasmic compartment was suffient to reduce Treg suppressive potency and fracture Treg-mediated maternal tolerance. Lastly, we identified that the expansion of Tregs during pregnancy was primed by fetal-specific antigens and resulted in a long-lived population of cells, which provide "regulatory" memory. This is the first demonstration of Tregs with the ability to re-expand following a secondary antigen challenge (either fetal or pathogen-derived) and should spark future investigation into the role of regulatory memory.
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    Roles of CD28, Inducible Costimulator, and the Interleukin-2 receptor in helper T cell memory formation.
    (2012-08) Pagan, Antonio Jose
    Numerous studies have suggested that CD28, Inducible Costimulator (ICOS), and Interleukin-2 receptor (IL-2R) signals shape the size and composition of the helper T cell memory pool, but the extent to which these signals regulate specific aspects of memory formation and the precise mechanisms of these processes remain unclear. To address this question, we used a sensitive peptide:Major Histocompatibility Complex II (p:MHCII) tetramer and magnetic bead-based enrichment method to track p:MHCII-specific helper T cells in mice throughout the course of an immune response. We found that CD28, ICOS, and the IL-2R each control unique aspects of helper T cell memory formation. The major defect in CD28-deficient T cells was a failure to sustain the proliferation of effector T cells and not a defect in memory formation per se; CD28-deficient T cells produced memory cells proportionate to the number of effectors present at the peak of the response. Our findings suggest that CD28 mediates this process by enhancing TCR-dependent NFκB signaling independently of the two CD28 cytoplasmic tail sequences previously implicated in clonal expansion. In contrast, ICOS or IL-2R deficiency did not grossly reduce the overall size of the effector or memory cell populations. Instead, they controlled the generation of two distinct subsets of memory T cells from effector cells that were present several days after infection. T-bethigh T helper type-1 effector memory (Th1em) cells were generated in an IL-2R-dependent fashion. In contrast, T-betlow CC chemokine receptor 7 (CCR7)+ CXC cheomokine receptor 5 (CXCR5)+ central memory T (Tcm) cells were formed in a Bcl6- and ICOS-dependent manner from T follicular helper (Tfh) effector cells. Thus, CD28, ICOS, and IL-2R regulate distinct aspects of helper T cell memory formation.
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    Using Genome-Scale Metabolic Models to Compare Serovars of the Foodborne Pathogen Listeria monocytogenes
    (2016-08) Metz, Zachary
    Listeria monocytogenes is a microorganism of great concern for the food industry, most notably because it is the 2nd most deadly bacterial foodborne pathogen. Therefore, it is important to study the organism in order to identify novel methods of control. Systems biology is one such approach. Using a combination of computational techniques and laboratory methods, genome-scale metabolic models (GEMs) can be created, validated, and used to simulate growth environments and discern metabolic capabilities of microbes of interest, including L. monocytogenes. The objective of the work presented here was to generate GEMs for six different strains of L. monocytogenes, and to both qualitatively and quantitatively validate these GEMs with experimental data. Qualitative validation by comparison to phenotypic microarray data resulted in GEMs with nutrient utilization agreement similar to that of previously published GEMs. Additionally, aerobic batch growth experiments resulted in predictions for growth rate and growth yield that were strongly and significantly correlated with experimental values. These findings are significant because they show that these GEMs for L. monocytogenes are comparable in agreement between in silico predictions and in vitro results to published models of other organisms. Therefore, as with the other models, namely those for Escherichia coli, Staphylococcus aureus, Vibrio vulnificus, and Salmonella spp., they can be used to determine new methods of growth control and disease treatment. Additionally, the findings confirm the acceptability of using semi-automated tools, like those provided by KBase, to generate GEMs.