Our mucosal surfaces are occupied by a robust and diverse ecosystem termed the commensal microbiome. When mucosal pathogens infect us, they first encounter our commensals before they encounter and activate our immune response.
We are interested in studying the interactions between the commensal microbiota, pathogens and the host immune response in the one place they must necessarily meet – the mucosa. Studying host-pathogen interactions at the mucosa allows us to identify novel pathways and mechanisms by which we resist or tolerate infections. We have multiple projects aimed at studying the mechanisms by which pathogens activate and evade the mucosal immune response and how these interactions are modulated by the microbiota. Our goal is to generate and test new ideas for vaccine and drug candidates to better protect people against infectious disease.
We're located at the Department of Immunology and Infectious Diseases at the Harvard T.H. Chan School of Public Health.
Unlike the intestinal microbiome, the vaginal microbiome consists of a smaller and more defined set of bacterial communities. The vaginal microbiome is also more consistent in people across the world, across diverse diets and ethnicities. Changes in the vaginal microbiome have been linked to increased susceptibility to and transmission of sexually transmitted infections. We are interested in bacterial community interactions of vaginal commensals and how this impacts host immunity to sexually transmitted diseases.
Gut-Vaginal Signaling Axis
The gut microbiome can influence distal sites in the body including the skin. We want to understand how the gut microbiome influences vaginal immune homeostasis. Conversely, it was recently discovered that genital herpes infections can result in viral infection of the enteric neurons in the colon. We will use this model to study how the vaginal immune response can prime and control immune responses to enteric viral infections.
Aminoglycoside Antiviral Signaling
We recently discovered that aminoglycosides (commonly used antibiotics) can induce antiviral gene transcription in dendritic cells, resulting in broad antiviral protection. We want to understand the intracellular signaling pathways involved, so we can build better antivirals.