Role of RelA and SpoT in Burkholderia pseudomallei survival, biofilm formation and ceftazidime tolerance during nutritional stress
Anutrakunchai, C; Hemsley, CM; Sermswan, RW; et al.Titball, RW; Chareonsudjai, S; Taweechaisupapong, S
Date: 1 December 2016
Journal
Tropical Biomedicine
Publisher
Malaysian Society of Parasitology and Tropical Medicine (MSPTM)
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Abstract
Burkholderia pseudomallei a saprophyte found in soil and stagnant water is the
causative agent of human melioidosis, an often cause fatal disease. B. pseudomallei is
intrinsically resistant to many antibiotics. The stringent response is a global bacterial adaptation
process in response to nutritional limitation and is mediated by ...
Burkholderia pseudomallei a saprophyte found in soil and stagnant water is the
causative agent of human melioidosis, an often cause fatal disease. B. pseudomallei is
intrinsically resistant to many antibiotics. The stringent response is a global bacterial adaptation
process in response to nutritional limitation and is mediated by the alarmone (p)ppGpp, which
is produced by two proteins, RelA and SpoT. In order to test whether the stringent response
is involved in ceftazidime tolerance, biofilm formation, and bacterial survival in the soil
microcosm, B. pseudomallei strain K96243 and its isogenic ΔrelA and ΔrelAΔspoT mutants
were grown in rich and nutrient-limited media. In nutrient-limiting conditions, both the wild
type and mutants were found to be up to 64-times more tolerant to ceftazidime than when
grown in rich culture conditions. Moreover, the biofilm formation of all bacterial isolates
tested were significantly higher under nutrient-limiting conditions than under nutrient-rich
conditions. The ΔrelAΔspoT mutant produced less biofilm than its wild type or ΔrelA mutant
under nutrient-limiting conditions. The survival of the ΔrelAΔspoT double mutant cultured in
1% moisture content soil was significantly decreased compared to the wild type and the ΔrelA
mutant. Therefore, the RelA/SpoT protein family might represent a promising target for the
development of novel antimicrobial agents to combat B. pseudomallei.
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