Current Protocols Molecular Biology 2010,

92:14.20.1–14.20.17. 54. Rasband W: ImageJ, U.S. Bethesda, Maryland, USA: National Institutes of Health; 1997–2012. http://​imagej.​nih.​gov/​ij/​ 55. R Core Team: R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing; 2012. http://​www.​R-project.​org 56. van Vliet S, Hol FJH, Weenink T, Galajda P, Keymer JE: The effects of chemical interactions and culture history on the colonization of structured habitats by competing bacterial populations. Data Set 2014. doi:10.4121/uuid:f5603abf-bf15–4732–84c0-a413ce7d12d3 Competing interests The authors declare that they have no competing interests. Authors’ contributions SvV participated in conceiving the study, participated in its design, performed the experiments and data Selleckchem CX5461 analysis and drafted the manuscript. FJHH contributed data analysis tools, helped to perform experiments, LGX818 mw and helped to draft the manuscript. TW performed exploratory experiments. PG performed exploratory Selleck HSP inhibitor experiments and participated in the design of the study. JEK conceived of the study, participated in its design and coordination and participated in drafting the manuscript. All authors read and approved the final manuscript.”
“Background Burkholderia pseudomallei, the causative agent of melioidosis, is a highly versatile Gram-negative bacterium capable of invading epithelial

cells [1] as well as surviving in macrophages [2]. Common routes of entry for B. pseudomallei are via cutaneous inoculation, inhalation, or ingestion. Melioidosis is endemic in Southeast Asia, Northern Australia and other tropical regions [3], and clinical outcome is relatively dependent on the size of the inoculum and the existence of predisposing risk factors [4]. B. pseudomallei possesses an extensive Cyclin-dependent kinase 3 arsenal

of recognized virulence determinants, including three “injection type” type III secretion systems (T3SSs) and six type VI secretion systems (T6SSs). T3SSs are present in many Gram-negative pathogens and translocate “effector” proteins into eukaryotic host cells to alter their cellular response. In B. pseudomallei, only T3SS3 has been implicated in animal pathogenesis [5, 6], while T3SS1 and −2 are predicted to mediate interactions with plants [7]. T3SS3 has also been shown to be important for bacterial escape from phagosomes or endosomes into the host cytosol [8, 9] and caspase 1-induced pyroptosis [10]. Since T3SS is a virulence determinant utilized by a variety of Gram-negative species, mammalian hosts have evolved sensors to detect the presence of T3SSs during pathogenesis. In macrophages, the T3SS of Salmonella typhimurium, Shigella flexneri, B. pseudomallei, Pseudomonas aeruginosa, enterohemorrhagic and enteropathogenic E. coli trigger a proinflammatory response mediated by the NLRC4 inflammasome and subsequent activation of caspase 1 [11].