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Category: Bacterial Pathogenesis
Type IV Secretion Systems and Their Role in Eliciting Host Responses to Infection, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555815851/9781555814694_Chap15-1.gif /docserver/preview/fulltext/10.1128/9781555815851/9781555814694_Chap15-2.gifAbstract:
Host responses elicited by type IV secretion systems (T4SS) activity are important factors in determining whether the infection will be resolved or whether bacteria will be able to cause a persistent infection. This chapter discusses recent findings on the functions of T4SS of Legionella pneumophila, Helicobacter pylori, Bordetella pertussis, Bartonella species, and Brucella species as well as new information gained from animal and cellular models of infection on how the secreted substrates alter the host’s response to infection. Legionella species are facultative intracellular pathogens found ubiquitously in freshwater environments, where they invade and replicate within amoebae and other protozoa. Importantly, NF- κB translocation is essential for the intracellular survival of Legionella, as the inhibition of this process resulted in the death of infected cells and prevented further bacterial replication when macrophages were infected at a low multiplicity of infection in a previous study. Studies of the global transcriptional response of gastric epithelial cells to H. pylori infection have shed light on the contribution of the T4SS to chronic inflammation and gastric cancer. Although the Dot/Icm T4SS transfers DNA by conjugation in vitro, it is not known whether DNA can be translocated into host cells during L. pneumophila infection. The popularity of employing T4SS for host-pathogen interaction may be due in part to the fact that these virulence factors can accommodate the secretion of distinct sets of effector proteins, thereby enabling each pathogen to adapt to a different specific niche.
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Assembly and function of the L. pneumophila Dot/Icm T4SS. ARF, ADP-ribosylation factor; CP, bacterial cytoplasm; CM, cytoplasmic membrane; PP, periplasm; OM, outer membrane; LPS, lipopolysaccharide; PM, plasma membrane; P-L, phagosome-lysosome. The assembly of the T4SS complex is inferred in part based on work on the A. tumefaciens T4SS, which is reviewed in references 10 and 24 .
Assembly and function of the H. pylori Cag PAI T4SS. PGN, peptidoglycan; P, phosphorylation. Other abbreviations are as defined in the legend to Fig. 1 . The assembly of the T4SS complex is inferred in part based on work on the A. tumefaciens T4SS, which is reviewed in references 10 and 24 .
Assembly and function of the Bartonella VirB T4SS. Abbreviations are as defined in the legend to Fig. 2 . The assembly of the T4SS complex is inferred in part based on work on the A. tumefaciens T4SS, which is reviewed in references 10 and 24 .
Animal and human pathogens and endosymbionts encoding T4SS
Motifs in T4SS effectors with similarity to eukaryotic protein domains