Primary prevention for resettled refugees from Burma: where to begin?

Developing effective primary prevention initiatives may help recently arrived refugees retain some of their own healthy cultural habits and reduce the tendency to adopt detrimental ones. This research explores recent arrivals' knowledge regarding eating behaviors, physical activity and sleep habits. Working collaboratively with community members, a healthy living curriculum was adapted and pilot tested in focus groups. A community-engaged approach to revising and implementing a health promotion tool was effective in beginning dialogue about primary prevention among a group of recently arrived refugees from Burma. Seven themes were identified as particularly relevant: food choices, living environment, health information, financial stress, mobility/transportation, social interaction and recreation, and hopes and dreams. Refugees desire more specific information about nutrition and exercise, and they find community health workers an effective medium for delivering this information. The outcomes of this study may inform future targeted interventions for health promotion with refugees from Burma.

Systemic disease during Streptococcus pneumoniae acute lung infection requires 12-lipoxygenase-dependent inflammation.

Acute pulmonary infection by Streptococcus pneumoniae is characterized by high bacterial numbers in the lung, a robust alveolar influx of polymorphonuclear cells (PMNs), and a risk of systemic spread of the bacterium. We investigated host mediators of S. pneumoniae-induced PMN migration and the role of inflammation in septicemia following pneumococcal lung infection. Hepoxilin A3 (HXA3) is a PMN chemoattractant and a metabolite of the 12-lipoxygenase (12-LOX) pathway. We observed that S. pneumoniae infection induced the production of 12-LOX in cultured pulmonary epithelium and in the lungs of infected mice. Inhibition of the 12-LOX pathway prevented pathogen-induced PMN transepithelial migration in vitro and dramatically reduced lung inflammation upon high-dose pulmonary challenge with S. pneumoniae in vivo, thus implicating HXA3 in pneumococcus-induced pulmonary inflammation. PMN basolateral-to-apical transmigration in vitro significantly increased apical-to-basolateral transepithelial migration of bacteria. Mice suppressed in the expression of 12-LOX exhibited little or no bacteremia and survived an otherwise lethal pulmonary challenge. Our data suggest that pneumococcal pulmonary inflammation is required for high-level bacteremia and systemic infection, partly by disrupting lung epithelium through 12-LOX-dependent HXA3 production and subsequent PMN transepithelial migration.