BORN TO WHEEZE OR LEARNED WHEN WE WERE YOUNG: MATERNAL AND ENVIRONMENTAL FACTORS INFLUENCE ATOPIC RISK

Abstract

The prevalence of atopic diseases is increasing globally, particularly in children. Heritable genetics can partially explain risk of disease. Evidence also points to acquired genetic material, in the form of the microbiome, as an important factor in disease pathogenesis. The acquisition of the microbiome dynamically changes in response to differences in lifestyle and environmental factors. Also, in utero, maternal and environmental factors influence atopic risk for allergic rhinitis, eczema, asthma, and food allergy. Combining the analytical power of omics, we focus on how the microbiota mediates effects between mother, environment, immunity, and risk of atopic disease. In parallel, we stress that health care disparities impact asthma morbidity and mortality. Efforts to improve asthma outcomes must include multidisciplinary strategies.

Fig. 1.

Lower Proteobacteria exposure is associated with increased risk of wheezing. (A) Kaplan-Meier curves for median of imputed cumulative percent parental reported wheezing at each year post-birth for children with high (solid, n=13) and low (dashed, n=10) exposure to Proteobacteria cfbDNA. (B) Children who had pulmonary function tests at mid-childhood follow-up (median age 8.0 years) were dichotomized for abundance of Proteobacteria, high (gray, n=4) and low (white, n=5). The groups were assessed for associations with changes in pulmonary function tests at mid-childhood. Bronchodilator response displayed as box and whisker plots for children with high or low (greater or less than the median, respectively) Proteobacteria exposure. P < 0.05 was considered statistically significant, Mann-Whitney U-test. From reference (1).

Fig. 2.

Extensive differences of network connectivity in tetanus toxoid-stimulated PBMCs in two-year-olds who are subsequently diagnosed with asthma. Pearson correlations between gene expression modules are displayed for the control (left) and asthmatic cohort (right), demonstrating utilization of different modules of genes in the two groups. Only statistically significant different edges are shown [p < 0.05 from Fisher's exact test comparing correlation coefficient (control and asthma), with edge thickness displayed as a function of strength of interaction]. From reference (2).

Fig. 3.

Albert Einstein riding a bicycle in front of Ben Meyer's house in Santa Barbara, California, Leo Baeck Institute, F 5314A.