Molds, parental atopy and pediatric incident asthma.

UNLABELLED: To assess the independent and joint effects of parental atopy and exposure to molds on the development of asthma in childhood, the authors conducted a cohort-based, incident case-control study in 2008. The case group consisted of 188 children with new asthma, and the control group (n=376) was matched one to two for age and sex. The outcome of interest was the development of asthma during the study period. The studied determinants were parental atopy and three indicators of exposure including histories of water damage, presence of visible molds, and perceived mold odor in the home at baseline in 2002. In conditional logistic regression adjusting for confounding, parental atopy [adjusted odds ratio (aOR) 3.29, 95% CI 2.19-4.94] and the presence of mold odor (aOR 2.09, 95% CI 1.30-3.37) and visible mold (aOR 1.76, 95% CI 1.18-2.62) were independent determinants of incident asthma, and apparent interaction in additive scale was observed. Our finding suggests that the interaction between parental atopy and molds may play a role in the development of asthma in children. PRACTICAL IMPLICATIONS: Our study strengthens the evidence for the roles of indoor dampness problem and parental atopy as determinants of asthma in children. Furthermore, the interaction between parental atopy and exposure to molds suggests a role for the development of childhood asthma, i.e., the children whose parents had atopic disease and molds exposure are more susceptible to develop asthma.

Identification and expression of scavenger receptor SR-BI in endothelial cells and smooth muscle cells of rat aorta in vitro and in vivo.

In this study, we used immunoelectron microscopy to investigate the subcellular localization of scavenger receptor class B type I (SR-BI) in the arterial walls of rats. The expression of SR-BI in cultured endothelial and smooth muscle cells of rat aorta after exposure to high-density lipoprotein (HDL) was also investigated by immunofluorescence microscopy and immunoblotting analysis. A peptide containing residues 495-509 from mouse SR-BI (mSR-BI) plus an NH2-terminal cysteine was coupled to hemocyanin to generate mSR-BI antiserum in rabbits. Reactivity of antiserum against the synthetic peptides was confirmed with an enzyme-linked immunosorbent assay (ELISA). The results showed that SR-BI was specifically localized on the surface of the endothelial cells and smooth muscle cells. SR-BI was also observed in the cytoplasm of smooth muscle cells. Immunoblotting analysis indicated that SR-BI was expressed in the cell membrane. The levels of SR-BI increased gradually from 1 to 3 h and decreased at 24 and 48 h after cholesterol-loaded cells were incubated in the culture medium containing HDL. We conclude that SR-BI, a functional receptor for HDL, is expressed in the aortic endothelial cells as well as in smooth muscle cells. This receptor also responds to the presence of HDL in the culture medium.