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interaction with human dendritic cells: phagocytosis, survival, and induced adaptive immune response are manipulated by PavA. J Immunol 2009, 183:1952–1963.PubMedCrossRef 43. Watanabe Y, Akizuki T: Prevention and treatment of penicillin-resistant Streptococcus pneumoniae meningitis after intracraniofacial surgery with distraction osteogenesis. Ispinesib supplier J Craniofac Surg 2008, 19:1542–1548.PubMedCrossRef 44. Wei BP, Robins-Browne RM, Shepherd RK, Clark GM, O’Leary SJ: Can we prevent cochlear implant recipients from developing pneumococcal meningitis? Clin Infect Dis 2008, 46:e1–e7.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions HM-R and WB-d-C conceived of the study. HM-R and AFB SGC-CBP30 molecular weight performed all experiments, except the isolation of the primary Schwann cell cultures. VTR-R and AC-R performed the primary Schwann cell cultures and the infection protocols. HM-R, AFB and LA participated in analyzing the data. HM-R, SA, VTR-R, LMT and WB-d-C participated in designing the study and wrote the final version of the manuscript.
LMT and WB-d-C participated in the design and coordination and helped to draft the manuscript. All authors read and approved the final manuscript.”
“Background Melioidosis is a serious and often fatal infectious disease common to Southeast Asia and Northern Australia caused by the Gram-negative soil bacterium Burkholderia pseudomallei. B. pseudomallei is a highly versatile pathogen capable of surviving inside mammalian cells and in many environmental niches. The bacterium can selleck inhibitor infect numerous animal species, amoebae, nematodes, and tomato plants [1–5], and has been previously found within the tissues of exotic
grasses in Australia [6]. The environmental origin of B. pseudomallei and its promiscuous host range have shaped the hypothesis that some of its genetic loci evolved in the rhizosphere as anti-predation determinants that subsequently promote “accidental” virulence in humans and animals. In recent years, important advances have been made in understanding the pathogenic mechanisms of B. pseudomallei including the roles of the Type III and Type VI Secretion Systems (T3SS, T6SS) [7–11]. B. pseudomallei contains three T3SSs Thiamet G and six T6SSs, but only T3SS3 (also referred to as the Burkholderia secretion apparatus, or T3SSBsa) and T6SS1 are critical for pathogenesis in mice and hamsters [7,12,13]. Expression of the T3SS3 and T6SS1 gene clusters is tightly controlled, both temporally and spatially, during the B. pseudomallei intracellular lifecycle. We have identified a regulatory cascade that coordinately activates T3SS3 and T6SS1 gene expression in growth medium and in infected mammalian cells [8,14]. At the top of the cascade is the TetR-type regulator BspR that stimulates the expression of bprP. The bspR gene is located on chromosome 1 of the B.