Virulence Factors That Modulate the Cell Biology of Listeria Infection and the Host Response
ABSTRACT The Gram-positive bacterial pathogen Listeria monocytogenes has become one of the best studied models in infection biology. This review will update our knowledge of Listeria virulence factors and highlight their role during the Listeria infection process.
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- "L. monocytogenes is considered an environmental pathogen as it is capable of life as a saprophyte in the outside environment while also maintaining the ability to invade and replicate within mammalian cells (Xayarath and Freitag, 2012). As part of the transition between life in the outside environment to life within the cytosol, L. monocytogenes increases the expression of secreted virulence factors that facilitate intracellular survival by promoting cell entry, bacterial escape from host vacuoles, replication within the cytosol, and spread to adjacent cells (Shetron-Rama et al., 2003; Mueller and Freitag, 2005; Port and Freitag, 2007; Alonzo and Freitag, 2010; de Las Heras et al., 2011; Mostowy and Cossart, 2012). The expression of many of the secreted virulence "
ABSTRACT: In Gram-positive bacteria, the secretion of proteins requires translocation of polypeptides across the bacterial membrane into the highly charged environment of the membrane-cell wall interface. Here, proteins must be folded and often further delivered across the matrix of the cell wall. While many aspects of protein secretion have been well studied in Gram-negative bacteria which possess both an inner and outer membrane, generally less attention has been given to the mechanics of protein secretion across the single cell membrane of Gram-positive bacteria. In this review, we focus on the role of a post-translocation secretion chaperone in Listeria monocytogenes known as PrsA2, and compare what is known regarding PrsA2 with PrsA homologs in other Gram-positive bacteria. PrsA2 is a member of a family of membrane-associated lipoproteins that contribute to the folding and stability of secreted proteins as they cross the bacterial membrane. PrsA2 contributes to the integrity of the L. monocytogenes cell wall as well as swimming motility and bacterial resistance to osmotic stress; however its most critical role may be its requirement for L. monocytogenes virulence and viability within host cells. A better understanding of the role of PrsA2 and PrsA-like homologs will provide insight into the dynamics of protein folding and stability in Gram-positive bacteria and may result in new strategies for optimizing protein secretion as well as inhibiting the production of virulence factors.Frontiers in Cellular and Infection Microbiology 02/2014; 4:13. DOI:10.3389/fcimb.2014.00013 · 2.62 Impact Factor
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ABSTRACT: Host defense against infection can broadly be categorized into systemic immunity and cell-autonomous immunity. Systemic immunity is crucial for all multicellular organisms, increasing in importance with increasing cellular complexity of the host. The systemic immune response to Listeria monocytogenes has been studied extensively in murine models; however, the clinical applicability of these findings to the human newborn remains incompletely understood. Furthermore, the ability to control infection at the level of an individual cell, known as "cell-autonomous immunity," appears most relevant following infection with L. monocytogenes; as the main target, the monocyte is centrally important to innate as well as adaptive systemic immunity to listeriosis. We thus suggest that the overall increased risk to suffer and die from L. monocytogenes infection in the newborn period is a direct consequence of age-dependent differences in cell-autonomous immunity of the monocyte to L. monocytogenes. We here review what is known about age-dependent differences in systemic innate and adaptive as well as cell-autonomous immunity to infection with Listeria monocytogenes.Clinical and Developmental Immunology 04/2013; 2013:917198. DOI:10.1155/2013/917198 · 2.93 Impact Factor
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ABSTRACT: Studies of CD8 T cell responses to vaccination or infection with various pathogens in both animal models and human subjects have revealed a markedly consistent array of age-related defects. In general, recent work shows that aged CD8 T cell responses are decreased in magnitude, and show poor differentiation into effector cells, with a reduced arsenal of effector functions. Here we review potential mechanisms underlying these defects. We specifically address phenotypic and numeric changes to the naïve CD8 T cell precursor pool, the impact of persistent viral infection(s) and inflammation, and contributions of the aging environment in which these cells are activated.Seminars in Immunology 05/2012; 24(5). DOI:10.1016/j.smim.2012.04.009 · 6.12 Impact Factor