Abstract
Many microorganisms produce phosphonates, molecules characterized by stable carbon-phosphorus bonds that store phosphorus or act as antimicrobials. The role of phosphonates in the marine biosphere is well characterized but the role of these molecules in the intestine is poorly understood. Salmonella enterica uses its virulence factors to influence the host immune response to compete with the host and normal microflora for nutrients. Salmonella cannot produce phosphonates but encodes the enzymes to use them suggesting that it is exposed to phosphonates during its life cycle. The role of phosphonates during enteric salmonellosis is unexplored. We have previously shown that STM3602, encoding a putative regulator of phosphonate metabolism, is needed for colonization in calves. Here, we report that the necessity of STM3602 in colonization of the murine intestine results from multiple factors. STM3602 is needed for full activation of the type-3 secretion system-1 and for optimal invasion of epithelial cells. The ΔSTM3602 mutant grows poorly in phosphonoacetic acid (PA) as the sole phosphorus source, but can use 2-aminoethylphosphonate. PhnA, an enzyme required for PA breakdown, is not controlled by STM3602 suggesting an additional mechanism for utilization of PA in S. Typhimurium. Finally, the requirement of STM3602 for intestinal colonization differs depending on the composition of the microflora. Our data suggest that STM3602 has multiple regulatory targets that are necessary for survival within the microbial community in the intestine. Determination of the members of the STM3602 regulon may illuminate new pathways needed for colonization of the host.
Highlights
In the intestine the microflora and the host vie for nutrients that vary in availability along the length of the intestine
Mice are treated with high doses of streptomycin prior to infection promoting Salmonella Typhimurium (STm) colonization and development of a neutrophilic inflammatory response
We found that the ∆STM3602 mutant is shed in lower numbers than the wild type organism in the feces by 24 h post-infection, and colonizes Peyer’s patches and mesenteric lymph nodes at lower levels than the wild type organism at 4 days post-infection (Figure 2)
Summary
In the intestine the microflora and the host vie for nutrients that vary in availability along the length of the intestine. Salmonella Typhimurium (STm) uses multiple strategies to gain nutrients and survive in this niche. STm uses host-derived sugars, such as ethanolamine released by microbial damage in the intestine, as energy sources during inflammation (Thiennimitr et al, 2011). Metal scavenging through salmochelin and high-affinity transporters allow STm to acquire essential nutrients during infection (Raffatellu et al, 2009; Liu et al, 2012). While these are some essential mechanisms salmonellae use to acquire nutrients and replicate in the intestine, these mechanisms may represent only a small fraction of the metabolic potential of STm in the intestine
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