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Response of Caenorhabditis elegans during Klebsiella pneumoniae pathogenesis

BMC Infectious Diseases201414 (Suppl 3) :P8

https://doi.org/10.1186/1471-2334-14-S3-P8

  • Published:

Keywords

  • Carbonyl
  • Virulent Gene
  • Antimicrobial Peptide
  • Innate Immune System
  • Caenorhabditis Elegans

Background

Caenorhabditis elegans, owing to its amenability and conserved innate immune system was recognized as an emerging model to dissect the molecular basis of many mammalian infections. Klebsiella pneumoniae causes severe infections in immunocompromised patients. Hence, the host response was studied using C. elegans during K. pneumoniae infection.

Methods

Pathogenicity of K. pneumoniae and its LPS were assessed by variety of physiological and biochemical assays. The qPCR was used to analyze the regulation of innate immune genes.

Results

K. pneumoniae and its LPS were lethal to C. elegans and required 48±5hours and 24±3hours for complete killing, respectively, with cessation of pharyngeal pumping and egg laying. Infection with K. pneumoniae increased the bacterial load in the intestine of host upon course of infection, which was measured as 1.5x103, 2.2x103, 3.6x104 and 3.7x105 in 4,6,12 and 24hours, respectively. This increased bacterial load subsequently disseminates oxidative stress markers in host. The level of ROS was measured to increase by 24.36597nM, 35.60517nM, 39.34052nM, and 28.24774 nM/mg of protein in 6, 12, 24, and 36 hours, respectively. Infection by K. pneumoniae also increased the protein carbonyls to 25.57nM, 36.14nM, 35.26nM and 38.84nM/mg of protein in 6, 12, 24, and 36 hours, respectively. K. pneumoniae and its LPS suppressed the expression of pmk-1, to l-1 and antimicrobial peptides (clec-60, clec-85, clec-87, lys-1, and lys-7) and thus succumbed the host by upregulated expression of virulent genes such as uge, rmpA and oxyR.

Conclusion

The interplay between K. pneumoniae and C.elegans in the present study further provides more insights into the mechanism of host defense against this pathogen.

Authors’ Affiliations

(1)
Department of Biotechnology, Alagappa University, Science Campus, Karaikudi, India

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