Allergic asthma is now regarded as the most common chronic respiratory disease to complicate pregnancy in Western countries. It has been established that women with moderate-severe asthma have an increased risk of worsening asthmatic disease during pregnancy. Furthermore, comprehensive meta-analysis studies have identified that moderate-severe asthma flare-ups in allergic atopic mothers throughout gestation increases the risk for low birth weight neonates, preterm delivery and the likelihood for the onset of non-communicable diseases, exemplified by the manifestation of allergic asthma during childhood.
Understanding the mechanisms that promote more severe asthmatic disease in pregnant mothers is limited by the absence of suitable animal models. The first phase of this study was to investigate whether sensitised mice undergoing chronic exposure to aeroallergen during pregnancy (i) develop increased inflammatory airways disease severity and (ii) whether this impacts fetal weight. Female BALB/c mice were sensitised or not with ovalbumin and adjuvant [Al(OH)3] before introduction to a BALB/c male. Once mating had been detected, sensitised pregnant mice were challenged with aeroallergen or saline 3 times weekly, with non-sensitised pregnant mice challenged with saline only. Maternal autopsy and fetal weight determination was carried out at multiple time points, 24h post last aerosol.
Following chronic aeroallergen challenge, both pregnant and non-pregnant sensitised mice displayed equivalent titres of serum OVA-specific IgE. While all sensitised mice responded to chronic aeroallergen challenge with increased total airways cellularity and proportion of eosinophils compared to non-sensitised mice, pregnancy was not associated with increased disease severity. Fetal weights at multiple time points after maternal autopsy were not significantly different between normal healthy pregnancies versus pregnant sensitised mice chronically exposed to aeroallergen throughout gestation. Adjusting the model to examine the above inflammatory parameters in response to acute aeroallergen exposure may subsequently provide a suitable model to elucidate the cellular mechanisms underlying increased asthmatic disease severity experienced during pregnancy.