Proteome analysis reveals translational inhibition of Caenorhabditis elegans enhances susceptibility to Pseudomonas aeruginosa PAO1 pathogenesis

Model system, C. elegans facilitates the identification of virulence mechanisms during bacterial pathogenesis. Upon infection by the fungal and bacterial pathogens, the C. elegans system induces an array of transcriptional responses, including differential expression of effector/modulator genes that provide safeguard and fight against infection. However, the in-depth knowledge of host response by the pathogen at protein level remains unclear. Much of the studies were carried out only at the transcripts level and scarce reports are available at the protein level for the host-pathogen interaction studies. In order to provide few interesting clues at the protein level, the nematode, C. elegans was infected with the human pathogen P. aeruginosa and the response(s) of host was investigated at the protein level by 2D-DIGE analysis and further validation studies using qPCR and western blotting techniques. Our differential proteomics data suggest that translational inhibition as one of the patterns of pathogenesis in C. elegans during P. aeruginosa infection. Since many of the effectors identified through C. elegans are conserved in other systems including human, our data pave the way for understanding important regulatory pathways involved during bacterial pathogenesis that can be translated into higher eukaryotic organisms.