Mucosal immunobiology and microbiology of food allergies
Our laboratory is interested in the role of the microbiota in shaping mucosal immunity and protection from food allergies. Epidemiologic and clinical data support the hypothesis that perturbations in the microbiota due to differences in "westernized" countries have disrupted the normal microbiota-mediated mechanisms of immunological tolerance in the mucosa, leading to an increase in the incidence of allergic diseases and other inflammatory conditions. Our laboratory demonstrated that mice can develop allergic responses to allergens if their endogenous microbiota is altered at the time of first allergen exposure. These experimental and clinical observations are consistent with other studies demonstrating that the endogenous microbiota plays a significant role in shaping the development of the immune system.

Candida albicans and Lactobacillus johnsonii studies
In conjunction with our mucosal immunity interest, our laboratory also studies the microbial ecology of mucosal surfaces and how colonization by the yeast Candida albicans and/or the bacterium Lactobacillus johnsonii can modify the response of the microbiome following antibiotic perturbation, as well as the downstream effects of colonization by these two microbes on regulation of mucosal immunity. Our goal is to study the molecular and cellular biology of this host-yeast-bacterial interaction in the gut.

Microbiome & respiratory diseases
With over 200 species, Pseudomonas is one of the largest, most genetically diverse and ecologically adaptable of all Gram-negative genera. Despite this diversity, the only Pseudomonas species recognized as a common colonizer of humans is the opportunistic pathogen Pseudomonas aeruginosa. However, non-aeruginosa Pseudomonas species (NAPS) can often be detected in clinical specimens, but they have been assumed to be clinically insignificant. We have ongoing studies in humans and mice that pulmonary inflammation results in a bloom of two NAPS in the lungs that have the potential to act as co-factors in chronic inflammation and disease, as demonstrated by in vitro, in vivo and in silico analyses.