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Infection and Immunity, November 2004, p. 6589-6596, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6589-6596.2004

Quorum Sensing: a Transcriptional Regulatory System Involved in the Pathogenicity of Burkholderia mallei

Ricky L. Ulrich,1* David DeShazer,1 Harry B. Hines,2 and Jeffrey A. Jeddeloh1*

Bacteriology Division,1 Toxinology/Aerobiology Division, United States Army Medical Research Institute of Infectious Diseases, Fort Detrick, Maryland2

Received 4 March 2004/ Returned for modification 19 April 2004/ Accepted 27 July 2004

Numerous gram-negative bacterial pathogens regulate virulence factor expression by using a cell density mechanism termed quorum sensing (QS). An in silico analysis of the Burkholderia mallei ATCC 23344 genome revealed that it encodes at least two luxI and four luxR homologues. Using mass spectrometry, we showed that wild-type B. mallei produces the signaling molecules N-octanoyl-homoserine lactone and N-decanoyl-homoserine lactone. To determine if QS is involved in the virulence of B. mallei, we generated mutations in each putative luxIR homologue and tested the pathogenicities of the derivative strains in aerosol BALB/c mouse and intraperitoneal hamster models. Disruption of the B. mallei QS alleles, especially in RJ16 (bmaII) and RJ17 (bmaI3), which are luxI mutants, significantly reduced virulence, as indicated by the survival of mice who were aerosolized with 104 CFU (10 50% lethal doses [LD50s]). For the B. mallei transcriptional regulator mutants (luxR homologues), mutation of the bmaR5 allele resulted in the most pronounced decrease in virulence, with 100% of the challenged animals surviving a dose of 10 LD50s. Using a Syrian hamster intraperitoneal model of infection, we determined the LD50s for wild-type B. mallei and each QS mutant. An increase in the relative LD50 was found for RJ16 (bmaI1) (>967 CFU), RJ17 (bmaI3) (115 CFU), and RJ20 (bmaR5) (151 CFU) compared to wild-type B. mallei (<13 CFU). These findings demonstrate that B. mallei carries multiple luxIR homologues that either directly or indirectly regulate the biosynthesis of an essential virulence factor(s) that contributes to the pathogenicity of B. mallei in vivo.

* Corresponding author. Mailing address for Ricky L. Ulrich: Bacteriology Division, USAMRIID, 1425 Porter St., Fort Detrick, MD 21702. Phone: (301) 619-8332. Fax: (301) 619-2152. E-mail: Ricky.Ulrich{at}amedd.army.mil. Present address for Jeffrey A. Jeddeloh: Orion Genomics, 4041 Forest Park, St. Louis, MO 63108. Phone: (314) 615-6382. Fax: (314) 615-6975. E-mail: jjeddeloh{at}oriongenomics.com.

Editor: J. B. Bliska

Infection and Immunity, November 2004, p. 6589-6596, Vol. 72, No. 11
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.11.6589-6596.2004




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