Under healthy conditions, the human body contains over 1014 bacteria. This number is about ten times higher than the estimated number of human cells in the body. Emerging evidence indicates that the interaction between the body and its microbiome is highly dynamic and can lead to many outcomes other than infectious diseases. Characterization of the molecular and cellular mechanisms at play in these interactions is providing a new understanding of microbial commensalism and pathogenicity.
Staphylococcus aureus (S. aureus) is carried chronically by over a quarter of healthy individuals without any ill effect. S. aureus is also a very common pathogen with a calculated health burden of $6 - 9 billion per year in the USA alone. This duality of outcomes makes S. aureus a pathobiont. We are using the interaction between S. aureus and the human immune system as a clinically relevant model to discover new regulatory mechanisms of immunity. Using a system immunobiology approach of S. aureus commensalism and infections, we are identifying those factors that determine the different result of encounters between this microbe and human beings.
In this talk, I will discuss our recent work leading to the identification of a TLR2-PI3K-Akt-dependent, IL-10-mediated response to glycopolymers embedded in the peptidoglycan layer of the cell wall of S. aureus (Nature Medicine 2009; 15: 6412; J Infect Dis 2011; 204: 253). Our preliminary data indicate that, depending on the site of interaction and the primary antigen-presenting cell, S. aureus can exploit this response to favor commensalism or pathogenicity. This knowledge may translate into future strategies to prevent and treat staphylococcal infections.
In addition, I will introduce the idea that evolutionary pressures may lead to selection of microorganisms towards symbiosis and ultimately probiotics, i.e. strains that have the capacity to modulate immunity in a beneficial way to the host (Int J Biochem Cell Biol 2010; 42: 1066).
Investigador de contacte:
Dr. Ricard Pujol