The Answer to Preventing Childhood Asthma: Found in Gut Microbes?

An infant’s sex-specific gut microbiome following maternal asthma during pregnancy may influence their risk of developing childhood asthma, according to a study published in the European Respiratory Journal.

The study, known as AllerGen’s CHILD Study and conducted by researchers from the University of Alberta, included 1000 mothers and their infants in a national population-based birth cohort.

The researchers determined that Caucasian boys born to women with asthma were one-third as likely to have a gut microbiome with specific characteristics at 3-4 months of age. These infants, who are typically at the highest risk for developing childhood asthma, were seen to have a reduced amount of Lactobacillus. The reduction was especially evident in infants born to mothers with asthma who had allergies or were overweight.

In girl infants, maternal asthma appeared to also influence gut bacteria. However, the researchers found that baby girls were more likely to have higher amounts of bacteria in the Bacteroidaceae family, which are important for protecting the gut from damage by harmful substances. The researchers noted that this may protect infant girls from developing early childhood asthma. However, they also noted that changes to bacterial composition specific to baby girls may increase their risk for developing asthma during puberty.

“Today, pregnant moms with asthma know they may pass along the disease to their infant,” Anita Kozyrskyj, PhD, study co-author, said in a press release. “But our discovery, with more research, could eventually lead to a prevention approach involving modifying the gut microbiome in infants to change the risk.”

However, she noted that it is still too early for parents to turn to probiotic treatments for their infants as an effort to prevent asthma development.

Reference

Koleva PT, Tun HM, Konya T, et al. Sex-specific impact of asthma during pregnancy in infant gut microbiota. Eur Respir J. 2017. doi: 10.1183/13993003.00280-2017.