Application of a novel socioeconomic measure using individual housing data in asthma research: an exploratory study.

BACKGROUND: A housing-based socioeconomic index (HOUSES) was previously developed to overcome an absence of socioeconomic status (SES) measures in common databases. HOUSES is associated with child health outcomes in Olmsted County, Minnesota, USA, but generalisability to other geographic areas is unclear. AIM: To assess whether HOUSES is associated with asthma outcomes outside Olmsted County, Minnesota, USA. METHODS: Using a random sample of children with asthma from Sanford Children's Hospital, Sioux Falls, SD, USA, asthma status was determined. The primary outcome was asthma control status using Asthma Control Test and a secondary outcome was risk of persistent asthma. Home address information and property data were merged to formulate HOUSES. Other SES measures were examined: income, parental education (PE), Hollingshead and Nakao-Treas index. RESULTS: Of a random sample of 200 children, 80 (40%) participated in the study. Of those, 13% had poorly controlled asthma. Addresses of 94% were matched with property data. HOUSES had moderate-good correlation with other SES measures except PE. Poor asthma control rates were 31.6%, 4.8% and 5.6% for patients in the lowest, intermediate and highest tertiles of HOUSES, respectively (P=0.023). HOUSES as a continuous variable was inversely associated with poorly controlled asthma (adjusted odds ratio (OR)=0.21 per 1 unit increase of HOUSES, 95% confidence interval (CI), 0.05-0.89, P=0.035). HOUSES as a continuous variable was inversely related to risk of persistent asthma (OR: 0.36 per 1 unit increase of HOUSES, 95% CI, 0.12-1.04, P=0.06). CONCLUSIONS: HOUSES appears to be generalisable and available as a measure of SES in asthma research in the absence of conventional SES measures.

Induction of MCP-1 expression in airway epithelial cells: role of CCR2 receptor in airway epithelial injury.

The repair of an injured bronchial epithelial cell (BEC) monolayer requires proliferation and migration of BECs into the injured area. We hypothesized that BEC monolayer injury results in monocyte chemoattractant protein-1 (MCP-1) production, which initiates the repair process. BECs (BEAS-2B from ATCC) were utilized in this study. MCP-1 interacts with CCR2B receptor (CCR2B), resulting in cell proliferation, haptotaxis, and healing of the monolayer. Reverse transcriptase-polymerase chain reaction (RT-PCR) was employed to verify the presence of CCR2B. CCR2B was not merely present but also inducible by interleukin-2 (IL-2) and lipopolysaccharide (LPS). We demonstrated by immunohistochemistry that BECs express MCP-1 after injury and that receptor expression can be regulated by exposure to IL-2 and LPS. Haptotactic migration of cells was enhanced in the presence of MCP-1 and reduced in the presence of CCR2B antibody. This enhanced or depressed ability of the BECs to perform haptotactic migration was shown to be statistically significant (P < 0.05) when compared to controls. Finally, BECs proliferate in response to MCP-1 as proven by electric cell-substrate impedance sensing (ECIS) technology. MCP-1-specific antibodies were shown to neutralize the MCP-1-mediated BEC proliferation. This cascade of events following injury to the bronchial epithelium may provide insight into the mechanism of the repair process.