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.

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.