Title: A P60 mutant of Listeria monocytogenes is impaired in its ability to cause infection in intragastrically inoculated mice Authors
|Faith, Nancy - UNIVERSITY OF WISCONSIN|
|Kathariou, Sophia - NORTH CAROLINA STATE|
|Neudeck, Brien - UNIVERSITY OF TENN.|
|Czuprynski, Charles - UNIVERSITY OF WISCONSIN|
Submitted to: Microbial Pathogenesis
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: January 22, 2007
Publication Date: February 4, 2007
Citation: Faith, N.G., Kathariou, S., Neudeck, B.L., Luchansky, J.B., Czuprynski, C.J. 2007. A p60 mutant of listeria monocytogenes is impaired in its ability to cause infection in intragastrically inoculated mice. Microbial Pathogenesis. 42:237-241. Interpretive Summary: Listeria monocytogenes, the causative agent of listeriosis, is found commonly in our food supply. This bacterium can cause serious illness for humans, particularly for people who are immunocompromised. We are conducting research to identify genetic material from within this organism which is responsible for its virulence. In this study we identified a strain with a spontaneous mutation in a gene termed p60. Compared to the parent strain, the p60 mutant strain was less able to establish an infection in mice following intragastric inoculation. Fewer cells of the mutant strain were recovered from internal organs and from the cecum of mice. In addition, the p60 mutant strain was also less able to invade and multiply within human intestinal epithelial cells under laboratory conditions. Our results indicate that the p60 gene is essential for pathogenicity of L. monocytogenes in the GI tract of mice.
Technical Abstract: A spontaneous P60 mutant of Listeria monocytogenes was less able to cause systemic infection in A/J mice, following intragastric inoculation, than the parental wild type strain (SLCC 5764, serotype 1/2a). Significantly fewer CFU were recovered from internal organs (spleen, liver, gall bladder) and from the cecum of mice inoculated intragastrically with the P60 mutant than mice inoculated with wild type L. monocytogenes. The P60 mutant also exhibited a diminished ability to invade and multiply within Caco-2 intestinal epithelial cells. These findings indicate that the P60 protein is required for maximal virulence of L. monocytogenes in the gastrointestinal tract of mice.