Air pollution: An environmental factor contributing to intestinal disease.

The health impacts of air pollution have received much attention and have recently been subject to extensive study. Exposure to air pollutants such as particulate matter (PM) has been linked to lung and cardiovascular disease and increases in both hospital admissions and mortality. However, little attention has been given to the effects of air pollution on the intestine. The recent discovery of genes linked to susceptibility to inflammatory bowel diseases (IBD) explains only a fraction of the hereditary variance for these diseases. This, together with evidence of increases in incidence of IBD in the past few decades of enhanced industrialization, suggests that environmental factors could contribute to disease pathogenesis. Despite this, little research has examined the potential contribution of air pollution and its components to intestinal disease. Exposure of the bowel to air pollutants occurs via mucociliary clearance of PM from the lungs as well as ingestion via food and water sources. Gaseous pollutants may also induce systemic effects. Plausible mechanisms mediating the effects of air pollutants on the bowel could include direct effects on epithelial cells, systemic inflammation and immune activation, and modulation of the intestinal microbiota. Although there is limited epidemiologic evidence to confirm this, we suggest that a link between air pollution and intestinal disease exists and warrants further study. This link may explain, at least in part, how environmental factors impact on IBD epidemiology and disease pathogenesis.

Altered sucrose metabolism impacts plant biomass production and flower development.

Nicotiana tabacum (tobacco) was transformed with three genes involved in sucrose metabolism, UDP-glucose pyrophosphorylase (UGPase, EC 2.7.7.9), sucrose synthase (SuSy, EC 2.4.1.13) and sucrose phosphate synthase (SPS, EC 2.4.1.14). Plants harbouring the single transgenes were subsequently crossed to produce double and triple transgenic lines, including: 2 x 35S::UGPase x SPS, 4CL::UGPase x SPS, 2 x 35S::SuSy x SPS, 4CL::SuSy x SPS, 2 x 35S::UGPase x SuSy x SPS, and 4CL::UGPase x SuSy x SPS. The ultimate aim of the study was to examine whether it is possible to alter cellulose production through the manipulation of sucrose metabolism genes. While altering sucrose metabolism using UGPase, SuSy and SPS does not have an end effect on cellulose production, their simultaneous overexpression resulted in enhanced primary growth as seen in an increase in height growth, in some cases over 50%. Furthermore, the pyramiding strategy of simultaneously altering the expression of multiple genes in combination resulted in increased time to reproductive bud formation as well as altered flower morphology and foliar stipule formation in 4CL lines. Upregulation of these sucrose metabolism genes appears to directly impact primary growth and therefore biomass production in tobacco.

Macrophage colony stimulating factor (CSF-1) is a central growth factor of goldfish macrophages.

We recently characterized macrophage colony stimulating factor (CSF-1) of fish (the goldfish). Here, we report for the first time that goldfish CSF-1 acts through the CSF-1 receptor by showing loss of CSF-1 function in CSF-1R knockdown monocytes using RNAi, and demonstrate that goldfish CSF-1 administration in vivo increases the amount of circulating monocytes in blood. We also show that conditioned supernatants from goldfish fibroblast cultures induced the proliferation of goldfish monocytes indicating that, like in mammals, teleost fibroblasts are an important producer of CSF-1. The continuous addition of recombinant CSF-1 to primary goldfish macrophage cultures stabilized and extended their longevity and resulted in a long-term culture of functional macrophages capable of mounting a potent nitric oxide response upon activation with goldfish recombinant TNF-alpha.