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Isolation and characterization of quorum-sensing signalling molecules in Pseudomonas aeruginosa isolates recovered from nosocomial infections

Authors

  • Krishnappa Lakshmana Gowda,

    1. Deparment of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Kingdom of Saudi Arabia
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  • James John,

    Corresponding author
    1. Department of Clinical Microbiology, Christian Medical College and Hospital, Vellore
    • Deparment of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Kingdom of Saudi Arabia
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    • These authors contributed equally to this work.
  • Mohammed A. M. Marie,

    1. Deparment of Clinical Laboratory Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Kingdom of Saudi Arabia
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  • Gopalkrishnan Sangeetha,

    1. Department of Microbiology, Central Leprosy Training and Research Institute, Chennai
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    • These authors contributed equally to this work.
  • Shanta Range Bindurani

    1. Department of Microbiology and Biochemistry, Shanthidhama College of Nursing Sciences, Bangalore, India
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James John, Department of Clinical Microbiology, Christian Medical College and Hospital, Vellore, Tamil Nadu 632004, India. e-mail: james_john3@rediffmail.com

Abstract

Pseudomonas aeruginosa is one of the most common pathogens in nosocomial infections. Many studies have documented the role of quorum-sensing (QS) systems in antibiotic tolerance of P. aeruginosa. N-acyl homoserine lactones (AHLs) serve as QS signalling molecules and can be a target for modulating bacterial pathogenicity. In this study, nosocomial isolates of P. aeruginosa were characterized for the presence of different types of QS signalling molecules. AHLs were solvent extracted and quantified by determination of β-galactosidase activity using the Escherichia coli MG4 reporter strain. Further characterization was performed by analytical thin layer chromatography coupled with detection using the Agrobacterium tumefaciens A136 biosensor strain. All P. aeruginosa isolates produced AHLs, but there were differences in the quantity and nature of AHLs. We identified AHLs belonging to C4-homoserine lactone (HSL), C6-HSL, C8-HSL, C10-HSL and C12-HSL. AHL profiling of P. aeruginosa isolates showed differences in the amounts and types of AHLs, suggesting differences in the virulence factors and the potential for infection. Our results may be investigated further using animal model systems.

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