The major focus of my laboratory is to understand the role of the NF-κB family of transcription factors in regulating innate inflammatory responses. NF-κB is generally thought of as a pro-inflammatory agent. However, work from our laboratory has demonstrated that certain NF-κB subunits inhibit the ability of bacteria to induce inflammation in several models, including mouse models for inflammatory bowel diseases and septic shock. Furthermore, NF-κB subunits also play a major role in limiting the ability of bacteria to induce critical pro-inflammatory genes such as IL-12. One of the mechanisms by which NF-κB subunits appear to inhibit pro-inflammatory gene expression is by facilitating the inhibitory potential of IL-10, a critical product of regulatory T cells. This may explain our observations that regulatory T cells are unable to suppress pathological inflammation in mice that lack NF-κB subunits.

Ongoing projects within the laboratory include elucidating the cellular and biochemical pathways by which NF-κB and IL-10 inhibit inflammatory bowel disease, and understanding the role of NF-κB subunits in regulating septic shock.