Research

Childhood undernutrition is a pervasive problem worldwide, resulting in reduced linear growth (stunting), increased risk of disease and cognitive defects that persist into adulthood. Maternal health profoundly influences fetal and childhood development; mothers that are stunted as children are more likely to give birth to stunted children themselves. Gut microbes influence growth and immune function, and the Cowardin lab is focused on investigating the role of the maternal and infant microbiota in shaping child health, with the goal of identifying specific microbial species and immune pathways for targeted intervention to reduce the global burden of undernutrition.

The lab has developed a model of intergenerational undernutrition using human microbial communities to colonize germ-free mice. Using this model, we have found that offspring derived from breeding pairs colonized with undernourished microbiota have altered growth and immune development when compared to offspring of breeders colonized with microbiota from a healthy donor.

Major questions arising from this work include:

1.     At what point in development is the gut microbiota critical for mediating healthy growth? Can we identify the optimal time to intervene to promote healthy development?

2.     Which microbial community members are responsible for differences in growth between healthy and undernourished offspring? Can we identify unique metabolic and genomic features of these organisms?

3.     What role does the maternal immune system’s response to gut microbes play in determining growth and development in early life? Can we reduce potentially damaging inflammatory responses, or promote healthy responses, to improve growth during undernutrition?

Answers to these questions have broad implications for child health and could influence susceptibility to intestinal infections common to underresourced settings, successful generation of vaccine responses (known to be reduced in children with undernutrition), and cognitive function later in life.