Abstract
Salmonella enterica is a common cause of diarrhea. For eliciting disease, the pathogen has to colonize the gut lumen, a site colonized by the microbiota. This process/initial stage is incompletely understood. Recent work established that one particular strain, Salmonella enterica subspecies 1 serovar Typhimurium strain SL1344, employs the hyb H2-hydrogenase for consuming microbiota-derived H2 to support gut luminal pathogen growth: Protons from the H2-splitting reaction contribute to the proton gradient across the outer bacterial membrane which can be harvested for ATP production or for import of carbon sources. However, it remained unclear, if other Salmonella strains would use the same strategy. In particular, earlier work had left unanswered if strain ATCC14028 might use H2 for growth at systemic sites. To clarify the role of the hydrogenases, it seems important to establish if H2 is used at systemic sites or in the gut and if Salmonella strains may differ with respect to the host sites where they require H2 in vivo. In order to resolve this, we constructed a strain lacking all three H2-hydrogenases of ATCC14028 (14028hyd3) and performed competitive infection experiments. Upon intragastric inoculation, 14028hyd3 was present at 100-fold lower numbers than 14028WT in the stool and at systemic sites. In contrast, i.v. inoculation led to equivalent systemic loads of 14028hyd3 and the wild type strain. However, the pathogen population spreading to the gut lumen featured again up to 100-fold attenuation of 14028hyd3. Therefore, ATCC14028 requires H2-hydrogenases for growth in the gut lumen and not at systemic sites. This extends previous work on ATCC14028 and supports the notion that H2-utilization might be a general feature of S. Typhimurium gut colonization.
Highlights
The gut lumen is colonized by a dense microbial community called the microbiota
low complexity microbiota (LCM) mice are ex-germfree C57BL/6 mice which had been colonized by the 8 strains of the altered Schadler flora and which had incorporated several dozen of additional strains into their microbiota during subsequent housing [8,9]
Typhimurium SL1344 can grow up in the gut lumen and reaches colonization densities of cfu/g by day 1 p.i., reaches cfu/g by day 3 and gut inflammation is triggered around day 3 p.i. [8]
Summary
The gut lumen is colonized by a dense microbial community called the microbiota. The microbiota performs numerous important functions which have been the topic of intense recent research (reviewed in [1]). ATCC14028 requires H2hydrogenases for growth in the gut lumen and not at systemic sites. Typhimurium strains to trigger membrane ruffling and elicit mucosal infection in cows and mice [33,34,35,36] the absence of SopE (or SopEW) was found to explain why ATCC14028 (but not SL1344) utilizes the terminal electron acceptor tetrathionate for anaerobic respiration in the lumen of the inflamed gut [37].
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