Salmonella polymicrobial interactions Abstract The normal microbiota provide essential nutrients and vitamins to the host and also make it very difficult for pathogenic microbes to colonize. It is well known that certain viral infections can facilitate secondary bacterial infections. However, the role that bacteria play in facilitating other bacterial infections is not well studied. We have determined that Salmonella encodes a LuxR homolog named SdiA that can detect the signaling molecules of other pathogenic bacteria in the host. To date, we have determined that Salmonella can detect Aeromonas hydrophila in turtles and Yersinia enterocolitica in mice and pigs. The ability of Salmonella to detect the signaling molecules of Yersinia in pigs led to a large increase in Salmonella shedding. In a separate study it was recently observed that swine infected with Yersinia enterocolitica are at increased risk to be colonized with Salmonella enterica. Given that Salmonella is one of the world's most significant pathogens, it is important to determine the parameters that lead to transmission of this organism. In this work, the extent to which a Yersinia infection increases the ability of Salmonella to colonize a host and be shed from that host will be determined. We will test the hypotheses that the infectious dose for Salmonella, the amount of Salmonella shed, and the persistence of Salmonella shedding are altered in a manner dependent upon the ability of Salmonella to detect the AHLs synthesized by Yersinia. The role of individual sdiA regulon members in each of these phenotypes will be determined. Additionally, array-based transposon screening will be used to identify novel Salmonella genes required to take advantage of coinfections. These genes will be parsed into sdiA- dependent and -independent groups, with the sdiA-dependent group being further categorized as to whether they are new members of the sdiA regulon or genes that act synergistically with sdiA. Relevance. The normal microbiota of the host play a very important role in preventing bacterial infections. The mechanisms by which pathogens circumvent or outcompete the normal microbiota are largely unknown. In this proposal we hypothesize that one method is to take advantage of another pathogen's success. Understanding the mechanisms by which pathogens interact with each other and with the normal microbiota will provide insights into pathogen host range and the ecology of disease and epidemics. This will facilitate the rational design and use of antibiotics and probiotics.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
7R01AI073971-03
Application #
7808091
Study Section
Bacterial Pathogenesis Study Section (BACP)
Program Officer
Alexander, William A
Project Start
2008-05-15
Project End
2013-04-30
Budget Start
2010-05-01
Budget End
2011-04-30
Support Year
3
Fiscal Year
2010
Total Cost
$578,600
Indirect Cost
Name
Ohio State University
Department
Microbiology/Immun/Virology
Type
Schools of Arts and Sciences
DUNS #
832127323
City
Columbus
State
OH
Country
United States
Zip Code
43210
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Gupta, Sushim K; McMillan, Elizabeth A; Jackson, Charlene R et al. (2016) Draft Genome Sequence of Salmonella enterica subsp. enterica Serovar Blockley Strain CRJJGF_00147 (Phylum Gammaproteobacteria). Genome Announc 4:
Gupta, Sushim K; McMillan, Elizabeth A; Jackson, Charlene R et al. (2016) Draft Genome Sequence of Salmonella enterica subsp. enterica Serovar Bardo Strain CRJJGF_00099 (Phylum Gammaproteobacteria). Genome Announc 4:
Gupta, Sushim K; McMillan, Elizabeth A; Jackson, Charlene R et al. (2016) Draft Genome Sequence of Salmonella enterica subsp. enterica Serovar Orion Strain CRJJGF_00093 (Phylum Gammaproteobacteria). Genome Announc 4:

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