In both wild-type (WT) and PGC-1 alpha KO mice liver, the mRNA content of the gluconeogenic proteins glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) was up-regulated during fasting. Pyruvate carboxylase (PC) remained BIBF 1120 Protein Tyrosine Kinase inhibitor unchanged after fasting in WT mice, but it was upregulated in PGC-1 alpha KO mice. In response to a single exercise bout, G6Pase mRNA was upregulated

in both genotypes, whereas no significant changes were detected in PEPCK or PC mRNA. While G6Pase and PC protein remained unchanged, liver PEPCK protein content was higher in trained than untrained mice of both genotypes. The mRNA content of the mitochondrial proteins cytochrome c (Cyt c) and cytochrome oxidase (COX) subunit Galardin ic50 I was unchanged in response to fasting. The mRNA and protein content of Cyt c and COXI increased in the liver in response to a single

exercise bout and prolonged exercise training, respectively, in WT mice, but not in PGC-1 alpha KO mice. Neither fasting nor exercise affected the mRNA expression of antioxidant enzymes in the liver, and knockout of PGC-1 alpha had no effect. In conclusion, these results suggest that PGC-1 alpha plays a pivotal role in regulation of Cyt c and COXI expression in the liver in response to a single exercise bout and prolonged exercise training, which implies that exercise training-induced improvements in oxidative capacity of the liver is regulated by PGC-1 alpha.”
“Extraintestinal pathogenic Escherichia coli can successfully colonize

the urinary tract of the immunocompetent host. In part, this is accomplished by dampening the host immune response. Indeed, the sisA and sisB genes (shiA-like inflammation suppressor genes A and B) of uropathogenic E. coli strain CFT073, homologs of the Shigella flexneri SHI-2 pathogenicity island gene shiA, suppress the host inflammatory response. A double deletion mutant (Delta sisA Delta sisB) resulted in a hyperinflammatory phenotype in an experimental model of ascending urinary tract infection. The Delta sisA Delta sisB mutant not only caused significantly more inflammatory foci find more in the kidneys of CBA/J mice (P = 0.0399), but these lesions were also histologically more severe (P = 0.0477) than lesions observed in mice infected with wild-type CFT073. This hyperinflammatory phenotype could be suppressed to wild-type levels by in vivo complementation of the Delta sisA Delta sisB mutant with either the sisA or sisB gene in trans. The Delta sisA Delta sisB mutant was outcompeted by wild-type CFT073 during cochallenge infection in the bladder (P = 0.0295) at 48 h postinoculation (hpi). However, during cochallenge infections, we reasoned that wild-type CFT073 could partially complement the Delta sisA Delta sisB mutant.