TANDEM – Section of Microbiology - University of Copenhagen

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Microbiology > Funded projects > TANDEM

Deciphering the causal mechanisms linking the early life microbiome and common chronic inflammatory diseases.

Groundbreaking novel results from the COPSAC2010 cohort suggest association between the gut microbial composition and the first year of life and the later risk of asthma. Thus, the microbiome may be an intermediary player in the interaction between the host and its environment in the extrinsic mechanisms that determine the transition from health to chronic disease.

Background and aim
The incidence of asthma and other chronic inflammatory diseases has more than doubled over the last century in the westernized world. It is a common working hypothesis that early microbiome interacts with the child's genetic makeup and that inappropriate microbiome composition can affect host immune maturation, thereby initiating a trajectory to immune mediated diseases such as asthma.
The overall aim in this project is to decipher the causal mechanisms linking the early life microbiome and common chronic inflammatory diseases. To do this, we aim at determining the full metagenome from gut and airways - before the onset of disease- and map the compositional-, functional- and metabolic potential of the microbiome to unravel the extrinsic mechanisms that determine the transition from health to chronic disease.

The COPSAC2010 cohort includes longitudinal deep clinical phenotyping, exposure assessment and biological samples from pregnancy through childhood. This provides a unique opportunity for deciphering the causal mechanisms linking the early life microbiome and common chronic inflammatory diseases facilitating determination of the healthy microbiome in early life and potentially also the possibility to identify key collaboromes (interspecies dependent microbiome consortia) which facilitate healthier composition.

Perspectives
If we succeed, this project could lay the foundation for understanding microbiota roles in development of chronic inflammatory diseases and potentially lead to novel prevention strategies and targeted, efficient microbiota manipulation in groups at risk.