Microbiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens

Ng, K.M. et al. Nature doi:10.1038/nature12503 (1 September)

The pathogens Salmonella enterica serovar Typhimurium and Clostridium difficile take advantage of host carbohydrates liberated by the actions of the microbiota, allowing them to expand in the mouse gut. Antibiotic treatment disrupted the host microbiota and increased the free amounts of pathogen-utilized carbohydrate, promoting expansion of the pathogenic bacteria.

Modified mRNA directs the fate of heart progenitor cells and induces vascular regeneration after myocardial infarction

Zangi, L. et al. Nat. Biotechnol. doi:10.1038/nbt.2682 (8 September)

Injection of a synthetic modified RNA encoding vascular endothelial growth factor-A improves heart function and survival in a mouse model of myocardial infarction.

A de novo gain-of-function mutation in SCN11A causes loss of pain perception

Leipold, E. et al. Nat. Genet. doi:10.1038/ng.2767 (15 September)

The authors identified a de novo missense mutation in the gene SCN11A, encoding a sodium channel, in people who cannot experience pain. They find that mice carrying this mutation show reduced sensitivity to pain and show that the mutation mediates its effects through a gain-of-function mechanism.

IL-27 acts on DCs to suppress the T cell response and autoimmunity by inducing expression of the immunoregulatory molecule CD39

Mascanfroni, I.D. et al. Nat. Immunol. doi:10.1038/ni.2695 (1 September)

Signaling by interleukin-27 (IL-27) in mouse dendritic cells suppresses T cell responses and the development of experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. These effects of IL-27 were partly mediated by its induction of CD39.

Brain tumor initiating cells adapt to restricted nutrition through preferential glucose uptake

Flavahan, W.A. et al. Nat. Neurosci. doi:10.1038/nn.3510 (1 September)

Nutrient restriction is shown to increase the survival of a population of cancer stem cells. These cells take up glucose efficiently by increasing their expression of the glucose transporter Glut3. Blocking Glut3 expression in the tumor-initiating cells reduced their growth and tumor progression when transplanted into mice.