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Title: BIOFILM FORMATION BY SALMONELLA ENTERICA SEROVAR TYPHIMURIUM ON HEP-2 CELLS AND CHICKEN INTESTINAL EPITHELIUM IS DEPENDENT ON AT LEAST FIVE FIMBRIAL GENE CLUSTERS

Author
item LEDEBOER, NATHAN - IOWA STATE UNIVERSITY
item Frye, Jonathan
item MCCLELLAND, MICHAEL - SIDNEY KIMMEL CANCER CTR
item JONES, BRAD - IOWA STATE UNIVERSITY

Submitted to: American Society for Microbiology Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 6/5/2005
Publication Date: 6/9/2006
Citation: Ledeboer, N.A., Frye, J.G., Mcclelland, M., Jones, B.D. 2006. Biofilm formation by salmonella enterica serovar typhimurium on hep-2 cells and chicken intestinal epithelium is dependent on at least five fimbrial gene clusters. American Society for Microbiology Meeting. May 21-25, 2006. Orlando, FL.

Interpretive Summary:

Technical Abstract: The ability of intestinal pathogens to establish themselves within the flora of the intestine is likely an important prerequisite for their ability to establish infection of a host. Based on the Salmonella genome sequence 14 putative fimbrial gene clusters have been identified. To determine the role of these fimbriae in biofilm formation on eukaryotic cell surfaces we have completed a microarray analysis and have identified genes from five different fimbrial gene clusters that are upregulated 5-fold or greater in biofilm. These gene clusters include: bovine colonization factor fimbriae (bcf), thin aggregative fimbriae (csg), long polar fimbriae (lpf), plasmid encoded fimbriae (pef), and the sth putative fimbrial operon. The role of these fimbrial operons in biofilm formation on chicken intestinal and HEp-2 cell surfaces was assayed using a modification of the once-flow-through-continuous culture system. Mutations in each fimbrial gene cluster demonstrated results varying from complete abrogation of biofilm formation to a slight increase in total biomass. Both the csg and pef mutations demonstrated a significant reduction to near complete loss in biofilm formed while the lpf mutation demonstrated a moderate loss of biofilm. The sth mutation had no effect in biofilm while the bcf mutation demonstrated a slight increase in biofilm formed on HEp-2 cells and a complete loss in biofilm formed on chicken intestine. Complementation of each mutation restored the ability to form biofilm. Based on these findings, we are continuing to investigate the role of fimbriae as well as extracellular polysaccharides in biofilm.