Document Type
Article
Language
eng
Publication Date
5-2012
Publisher
Public Library of Science
Source Publication
PLoS One
Source ISSN
1932-6203
Original Item ID
doi: 10.1371/journal.pone.0038200
Abstract
Vibrio cholerae cytolysin (VCC) is among the accessory V. cholerae virulence factors that may contribute to disease pathogenesis in humans. VCC, encoded by hlyA gene, belongs to the most common class of bacterial toxins, known as poreforming toxins (PFTs). V. cholerae infects and kills Caenorhabditis elegans via cholerae toxin independent manner. VCC is required for the lethality, growth retardation and intestinal cell vacuolation during the infection. However, little is known about the host gene expression responses against VCC. To address this question we performed a microarray study in C. elegans exposed to V. cholerae strains with intact and deleted hlyA genes. Many of the VCC regulated genes identified, including C-type lectins, Prion-like (glutamine [Q]/asparagine [N]-rich)-domain containing genes, genes regulated by insulin/ IGF-1-mediated signaling (IIS) pathway, were previously reported as mediators of innate immune response against other bacteria in C. elegans. Protective function of the subset of the genes up-regulated by VCC was confirmed using RNAi. By means of a machine learning algorithm called FastMEDUSA, we identified several putative VCC induced immune regulatory transcriptional factors and transcription factor binding motifs. Our results suggest that VCC is a major virulence factor, which induces a wide variety of immune response- related genes during V. cholerae infection in C. elegans.
Recommended Citation
Sahu, Surasri N.; Lewis, Jada; Patel, Isha; Bozdag, Serdar; Lee, Jeong H.; LeClerc, Joseph E.; and Cinar, Hediye Nese, "Genomic Analysis of Immune Response against Vibrio Cholerae Hemolysin in Caenorhabditis elegans" (2012). Mathematics, Statistics and Computer Science Faculty Research and Publications. 100.
https://epublications.marquette.edu/mscs_fac/100
Comments
Published version. PLoS One, Vol. 7, No. 5 (May, 2012): e38200. Permalink © 2012 Public Library of Science. Used with permission.