ASU Scholarship Showcase

Salmonella enterica serovar Typhimurium strains belonging to sequence type ST313 are a major cause of fatal bacteremia among HIV-infected adults and children in sub-Saharan Africa. Unlike “classical” non-typhoidal Salmonella (NTS), gastroenteritis is often absent during ST313 infections and isolates are most commonly recovered from blood, rather than from stool. This is consistent with observations in animals, in which ST313 strains displayed lower levels of intestinal colonization and higher recovery from deeper tissues relative to classic NTS isolates. A better understanding of the key environmental factors regulating these systemic infections is urgently needed. Our previous studies using dynamic Rotating Wall Vessel (RWV) bioreactor technology demonstrated that physiological levels of fluid shear regulate virulence, gene expression, and stress response profiles of classic S. Typhimurium. Here we provide the first demonstration that fluid shear alters the virulence potential and pathogenesis-related stress responses of ST313 strain D23580 in a manner that differs from classic NTS.

Vertebrates cannot synthesize carotenoid pigments de novo, so to produce carotenoid-based coloration they must ingest carotenoids. Most songbirds that deposit red carotenoids in feathers, bills, eyes, or skin ingest only yellow or orange dietary pigments, which they oxidize to red pigments via a ketolation reaction. It has been hypothesized that carotenoid ketolation occurs in the liver of vertebrates, but this hypothesis remains to be confirmed. To better understand the role of hepatocytes in the production of ketolated carotenoids in songbirds, we measured the carotenoid content of subcellular components of hepatocytes from wild male house finches (Haemorhous mexicanus) that were molting red, ketocarotenoid-containing feathers (e.g., 3-hydroxy-echinenone). We homogenized freshly collected livers of house finches and isolated subcellular fractions, including mitochondria. We found the highest concentration of ketocarotenoids in the mitochondrial fraction. These observations are consistent with the hypothesis that carotenoid pigments are oxidized on or within hepatic mitochondria, esterified, and then transported to the Golgi apparatus for secretory processing.