Genome Sequences of 12 Bacterial Isolates Obtained from the Urine of Pregnant Women.

The presence of bacteria in urine can pose significant risks during pregnancy. However, there are few reference genome strains for many common urinary bacteria. We isolated 12 urinary strains of Streptococcus, Staphylococcus, Citrobacter, Gardnerella, and Lactobacillus These strains and their genomes are now available to the research community.

Host-like carbohydrates promote bloodstream survival of Vibrio vulnificus in vivo.

Sialic acids are found on all vertebrate cell surfaces and are part of a larger class of molecules known as nonulosonic acids. Many bacterial pathogens synthesize related nine-carbon backbone sugars; however, the role(s) of these non-sialic acid molecules in host-pathogen interactions is poorly understood. Vibrio vulnificus is the leading cause of seafood-related death in the United States due to its ability to quickly access the host bloodstream, which it can accomplish through gastrointestinal or wound infection. However, little is known about how this organism persists systemically. Here we demonstrate that sialic acid-like molecules are present on the lipopolysaccharide of V. vulnificus, are required for full motility and biofilm formation, and also contribute to the organism's natural resistance to polymyxin B. Further experiments in a murine model of intravenous V. vulnificus infection demonstrated that expression of nonulosonic acids had a striking benefit for bacterial survival during bloodstream infection and dissemination to other tissues in vivo. In fact, levels of bacterial persistence in the blood corresponded to the overall levels of these molecules expressed by V. vulnificus isolates. Taken together, these results suggest that molecules similar to sialic acids evolved to facilitate the aquatic lifestyle of V. vulnificus but that their emergence also resulted in a gain of function with life-threatening potential in the human host.

Effects of high-density lipoprotein on endothelium-dependent vasorelaxation.

Studies using cultured endothelial cells have shown that high-density lipoprotein (HDL) positively modulates endothelial nitric oxide synthase (eNOS). The purpose of this study was to test the hypotheses that positive modulation of eNOS by HDL occurs in whole vessels and that it augments endothelium-dependent vasorelaxation. To test these hypotheses, brachial arteries were obtained from swine. Endothelium-dependent and endothelium-independent vasorelaxation were determined in vitro to assess the effects of acute administration of HDL (50 microg.mL-1; n = 8) and chronic exposure to relatively high HDL concentration on vascular function (low HDL, 0.89 +/- 0.02 mmol.L-1, n = 4; high HDL, 1.16 +/- 0.05 mmol.L-1, n = 4; p < 0.005). Acute administration of HDL did not augment maximal endothelium-dependent vasorelaxation to bradykinin (BK) (no HDL, 82.6% +/- 2.2%; HDL, 76.7% +/- 3.5%; not significant (ns)). Similarly, maximal relaxation to BK was not enhanced by chronic exposure to high HDL concentrations. NO synthase (NOS) activity was also similar between groups (low HDL, 129.0 +/- 19.2 counts.h-1.microg-1 protein; high HDL, 113.9 +/- 47.1 counts.h-1.microg-1; ns). Consistent with NOS activity, the extent of eNOS phosphorylation at several sites was similar between low HDL and high HDL. Both apolipoprotein A-I (ApoA-I) and scavenger receptor class B type I (SR-BI) were associated with eNOS. Similar to cultured cell studies, this study demonstrates that both ApoA-I and SR-BI associate with eNOS in the vascular wall. Binding of ApoA-I and SR-BI to eNOS does not, however, result in modulation of either NO formation or endothelial function.