Among serious and chronic childhood diseases, asthma is the most prevalent. Currently there exists no cure for asthma—only treatments designed to help manage symptoms. Recently, a body of research attempting to unravel how this condition develops in young children has emerged, so that prevention may one day eliminate or reduce the burden of this chronic condition.
Recent work identified the existence of a critical window during the early lives of both mice and children, during which gut microbial changes are associated with the development of asthma. This provided an avenue to explore the role of the gut microbiome during early childhood development and the onset of chronic diseases like asthma. Importantly though, we know the gut microbiome varies greatly among those raised in different geographic regions. Therefore, understanding how changes in gut microbiota related to asthma development differ globally may provide valuable insights into the mechanism of asthma development.
A new paper, led by Microbiome Insights co-founder Brett Finlay and published in The Journal of Allergy and Clinical Immunology, evaluated the associations of fungal and bacterial changes (dysbiosis) in infants raised in the non-industrialized setting of rural Ecuador. The research was conducted as a collaboration between members of the Universities of British Colombia and Calgary, the BC Children’s Hospital, and Universidad Internacional del Ecuador. Children with atopic wheeze (27 in total) along with 70 healthy controls were identified and their bacterial and eukaryotic gut microbiota analysed at age 3 months. Stool samples were collected and sequencing of the 16S and 18S regions predicted bacterial metagenomes while fecal short chain fatty acids were determined via gas chromatography.
Results indicated that, similar to the previous findings in Canadian children, microbial dysbiosis in Ecuadorian infants at 3 months was associated with the subsequent development of atopic wheeze. Surprisingly though, the dysbiosis observed in Ecuador involved different bacteria taxa as well as some fungal species, and this was more pronounced than in Canada. Some predictions based on the metagenome analysis also emphasized significant dysbiosis-associated differences in genes involved in carbohydrate and taurine metabolism. The fecal short-chain fatty acid acetate was reduced while caproate was increased in children at 3 months who later developed atopic wheeze.
This work continues to provide evidence that there is a critical window during the first 100 days of life during which microbial dysbiosis is strongly associated with development of atopic wheeze. The study also yielded several valuable pieces of information. Despite the involvement of different bacteria taxa, both the Canadian and Ecuadorian populations had decreased fecal acetate, suggesting alterations to fermentation patterns may be a common factor associated with atopic wheeze. Furthermore, the pronounced role of fungal dysbiosis in this study led researchers to recommend that “the role of P. kudriavzevii and other yeasts should be explored in mechanistic studies using animal models.”
Along with more studies characterizing the early microbiome in more communities around the world, optimized biomarker studies of microbial taxa and metabolites could lead to better predictions of risk and therapeutic strategies to restore gut microbial health as a prevention method.