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Title: Motility revertants of opgGH mutants of Salmonella enterica serovar Typhimurium remain defective in mice virulence

Author
item KANNAN, PORTEEN - Indian Veterinary Research Institute
item DHARNE, MAHESH - University Of Poona
item Smith, Allen
item Karns, Jeffrey
item Bhagwat, Arvind

Submitted to: Current Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/7/2009
Publication Date: 10/10/2009
Citation: Kannan, P., Dharne, M., Smith, A.D., Karns, J.S., Bhagwat, A.A. 2009. Motility revertants of opgGH mutants of Salmonella enterica serovar Typhimurium remain defective in mice virulence. Current Microbiology. 59(6):641-645.

Interpretive Summary: The ability to survive under low nutrient conditions in the environment enables Salmonella spp. to successfully enter the food chain. Vegetable wash waters and irrigation waters have been implicated in recent outbreaks of infections caused by Salmonella spp. In this study we show that the ability to make specific glucose-polymer by Salmonella strains under nutritionally challenging conditions is crucial for its virulence. Salmonella strains synthesizing this glucose-polymer were more virulent in mice. Understanding how pathogens overcome various stress conditions such as low nutrient environments will advance our knowledge of how enteric human pathogens enter our food chain. The research will benefit the fresh produce industry, as well as increasing the microbial food safety of the Americans food supply.

Technical Abstract: We recently demonstrated that osmoregulated periplasmic glucans (OPGs) of Salmonella enterica serovar Typhimurium are required for optimal mouse virulence (Bhagwat et al., 2009. Microbiology 155:229-237). However, lack of OPGs also generated pleiotropic phenotypes such as reduced motility and slower growth rate under hypoosmotic growth conditions. Whether the observed suboptimal virulence of opg mutants was due to reduced motility was investigated by isolating fully motile revertants of opgGH mutants. Motility revertants remained defective in OPGs synthesis and continued to show longer lag period when grown under hypoosmotic conditions. Restitution of motility did not restore mouse virulence. In E. coli, lack of OPGs biosynthesis has been documented to trigger the induction of the Rcs phosphorelay pathway which is speculated to be the primary cause of motility suppression. In Salmonella strains, activation of the Rcs pathway is known to attenuate virulence. No significant differences in the transcript levels of the Rcs pathway genes were detected in opgGH mutants and revertant strain. Except for two silent mutations no other changes in the DNA sequences of Rcs genes were detected in the revertant strain. The data suggest a more direct role for OPGs in host-microbe interactions and the likely involvement of regulatory elements other than Rcs genes in controlling motility and virulence in opg mutants.