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Infection and Immunity, October 1999, p. 5324-5331, Vol. 67, No. 10
Department of Microbiology and Immunology,
University of Arkansas for Medical Sciences, Little Rock, Arkansas
72205
Received 8 April 1999/Returned for modification 10 June
1999/Accepted 9 July 1999
Burn wounds are prone to infection by Pseudomonas
aeruginosa, which is an opportunistic pathogen causing various
human diseases. During infection, the bacterium senses environmental
changes and regulates the expression of genes appropriate for survival.
A purine-auxotrophic mutant of P. aeruginosa was unable to
replicate efficiently on burn wounds, suggesting that burn wounds are
purine-deficient environments. An in vivo expression technology based
on purEK gene expression was applied to the burned mouse
infection model to isolate P. aeruginosa genes that are
specifically induced during infection. Four such in vivo-inducible
(ivi) genetic loci were identified, including the gene for
a superoxide response regulator (soxR), the gene for a
malate synthase G homologue (glcG), an antisense transcript
of a putative regulator responding to copper (copR), and an
uncharacterized genetic locus. SoxR of Escherichia coli is
known to regulate genes involved in protecting the bacterium against
oxidative stress. The expression of soxR was proven to be
highly inducible during the infection of burned mice and also inducible
by treatment with paraquat, which is a redox-cycling reagent generating
intracellular superoxide. The SoxR protein functions as an
autorepressor in the absence of paraquat, whereas in the presence of
paraquat, this autorepression is diminished. Furthermore, a
soxR null mutant was shown to be much more sensitive than
wild-type P. aeruginosa to macrophage-mediated killing. In support of this observation, a soxR null mutant exhibited a
significant delay in causing systemic infections in the burned mice.
Since most mortality in burn patients is caused by systemic infection, the defect in the ability to cause efficient bacteremia in burned mice
suggests an important role of the soxR gene in the
infection of burn wounds.
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Expression of the soxR Gene of
Pseudomonas aeruginosa Is Inducible during Infection of
Burn Wounds in Mice and Is Required To Cause Efficient
Bacteremia
*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, University of Arkansas for Medical
Sciences, 4301 West Markham, Slot 511, Little Rock, AR 72205-7199. Phone: (501) 296-1396. Fax: (501) 686-5359. E-mail:
jinshouguang{at}exchange.uams.edu.
Infection and Immunity, October 1999, p. 5324-5331, Vol. 67, No. 10
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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