About this Research Topic
L. monocytogenes has long been used as a model pathogen in infectious disease research. These studies have led to important discoveries and paradigm shifts in immunology and cellular microbiology. In particular, the development of the mouse model of L. monocytogenes infection has made a critical contribution to the discovery of cell-mediated immune response against intracellular bacteria. Analysis of the L. monocytogenes intracellular lifecycle in cultured cells has revealed fundamental mechanisms that orchestrate bacterial internalization into host cells, exit from the endocytic vesicle, intracellular proliferation, and motility leading to bacterial spread from cell to cell. Not only has L. monocytogenes enhanced our understanding of bacterial biology, but also it has been instrumental in studying eukaryotic cell biology. This is well illustrated by advances made in the identification and elucidation of the mechanisms of action of noncoding RNAs in bacterial and eukaryotic cells during infection, as well as in understanding the mechanisms that control cytoskeletal assemblies in eukaryotic cells. One of the most important challenges now is to elucidate molecular mechanisms that control the L. monocytogenes interaction with the gut microbiota and the pathogen-host cell interplay in vivo during pathogenesis. In this line of investigation, the use of animal models of L. monocytogenes infection confirmed some molecular pathways that were initially discovered in cell culture models, and also led to the discovery of unexpected routes used by the pathogen to infect its host. Finally, the advent of “omic” technologies is providing comprehensive information on the regulation of the host-pathogen interplay during pathogenesis. Given the fascinating biology of L. monocytogenes and its intricate interplay with its hosts, there is no doubt that studies on this pathogen will generate many more discoveries.
This research topic aims to broadly address the biology and pathogenesis of Listeria monocytogenes. Original research manuscripts, methods, opinions, reviews, and mini reviews will be received until September 2013.
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