The gut harbors most of the body’s immune cells, and its development requires a sequential series of events starting in the prenatal period. Disruptions to these events can result in altered immune function, with long-term implications for host inflammatory responses. Microbial colonization is an important contributor to early immune development. Animal studies show that pre and postnatal stress affect both microbial colonization patterns and host inflammatory responses. In humans, inflammation has been identified as an important mechanism by which the stress of psychosocial adversity becomes “biologically embedded”, leading to disparities in health outcomes. This proposal tests the hypothesis that the gut microbiome as a critical intermediary between host systemic inflammatory response and pre- and postnatal psychosocial stress in early childhood.
Proposed specific aims
· Determine if microbial content shifts in the gut precede the development of the pro-inflammatory state.
· Confirm or refute the role of pre- and postnatal psychosocial stress in the development of the childhood gut microbiome, in the context of associated host inflammation.
Potential impact on child health
Importantly, this project provides the first human examination of the effects of the gut microbiome and biomarkers of inflammation studied in the context of psychosocial adversity. Results from this study may be used to develop strategies to improve immune-mediated health outcomes of children.
Phillip Tarr, M.D.