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Applied and Environmental Microbiology, July 2008, p. 4185-4198, Vol. 74, No. 13
0099-2240/08/$08.00+0     doi:10.1128/AEM.00381-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Virulence of Leucobacter chromiireducens subsp. solipictus to Caenorhabditis elegans: Characterization of a Novel Host-Pathogen Interaction ^,

Department of Genetics,¹ Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305²

Received 14 February 2008/ Accepted 1 May 2008

We describe the pathogenic interaction between a newly described gram-positive bacterium, Leucobacter chromiireducens subsp. solipictus strain TAN 31504, and the nematode Caenorhabditis elegans. TAN 31504 pathogenesis on C. elegans is exerted primarily through infection of the adult nematode uterus. TAN 31504 enters the uterus through the external vulval opening, and the ensuing uterine infection is strongly correlated with a significant reduction in host life span. Young worms can feed and develop on TAN 31504, but not preferably over the standard food source. C. elegans worms reared on TAN 31504 as the sole food source develop into thin adults with little intestinal fat stores, produce few progeny, and subsequently cannot persist on the pathogenic food source. Within 12 h of exposure, adult worms challenged with TAN 31504 alter the expression of a number of C. elegans innate immunity-related genes, including nlp-29, which encodes a neuropeptide-like protein. C. elegans worms exposed briefly to TAN 31504 develop lethal uterine infections analogous to worms exposed continuously to pathogen, suggesting that mere contact with the pathogen is sufficient for the host to become infected. TAN 31504 produces a robust biofilm, and this behavior is speculated to play a role in the virulence exerted on the nematode host. The interaction between TAN 31504 and C. elegans provides a convenient opportunity to study bacterial virulence on nematode tissues other than the intestine and may allow for the discovery of host innate immunity elicited specifically in response to vulva-uterus infection.

Published ahead of print on 16 May 2008.

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