Gene 2009, 430:123–131.PubMedCentralPubMedCrossRef 75. DeShazer D, Brett PJ, Carlyon R, Woods DE: Mutagenesis of Burkholderia pseudomallei with Tn5-OT182: isolation of motility mutants and molecular characterization of the flagellin structural gene. J Bacteriol 1997, 179:2116–2125.PubMedCentralPubMed 76. Ulrich RL, Amemiya K, Waag DM, Roy CJ, DeShazer D: Aerogenic vaccination with a Burkholderia mallei auxotroph protects

against aerosol-initiated glanders in mice. Vaccine 2005, 23:1986–1992.PubMedCrossRef Competing interests G. Pegoraro www.selleckchem.com/products/mk-5108-vx-689.html was a PerkinElmer employee. Authors’ contributions GP: designed and developed the image acquisition and analysis procedures; DD constructed the Bp ∆bsaZ mutant; BE, DL, JO performed all the experiments, RGP conceived the experimental https://www.selleckchem.com/products/wnt-c59-c59.html design and drafted the manuscript; SB, RU and DD provided critical review of the manuscript. All authors contributed to writing the manuscript and read and approved the final version.”
“Background Cytolethal distending toxin (CDT) was discovered in an Escherichia coli strain isolated from diarrheal patient in 1987 [1]. Since then, expression of CDT has been reported from a variety of pathogenic Gram-negative bacteria, including Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans, Campylobacter spp., Escherichia albertii, Haemophilus

ducreyi, Helicobacter spp., Providencia alcalifaciens, and Shigella spp. [2–4]. The cdt operon contains three adjacent genes, cdtA, cdtB and cdtC, and expression of all the genes is necessary for maximum toxin activity. While CdtB acts as an active subunit with DNase I activity, CdtA and CdtC facilitate binding of CDT to a yet-to-be-identified receptor molecule(s) on susceptible cells and entry of CdtB into the BIBF 1120 mw cytoplasm. As a result, CDT induces distention and eventual death of certain cultured eukaryotic cell lines by causing an irreversible

arrest of the cell cycle at the G1 or G2 phase [4]. In CDT-producing E. coli (CTEC), five subtypes of CDT (I through V) have been reported based on the amino acid sequences and the genomic location of their genes [4]. Although CTEC strains have been isolated from children with diarrhea [4], case control studies conducted in children up to 5 years of age in Brazil (used DNA probes for CDT-I) [5], Bangladesh (for CDT-I) [6] and Nigeria acetylcholine (for CDT-I and CDT-II) [7] failed to demonstrate significant association of CTEC with acute diarrhea. However, animal experiments with recombinant CDT of Shigella dysenteriae and Campylobacter jejuni CDT knockout mutants indicated that CDT is involved in diarrhea and inflammatory response [2]. Moreover, Pandey et al. [8] reported that high titer CDT-I-producing enteropathogenic E. coli (EPEC) were isolated from patients with bloody diarrhea in India while low titer producers were isolated from patients with acute watery diarrhea. We also demonstrated that an E.