Research Description

All projects in the lab are centered on understanding the inflammation-immune response to stimuli ranging from mechanical and chemical to pathogenic. In this direction, our interest has been on the vascular system which serves as the converging site for inflammation; indeed, the endothelium that lines the vascular system is where immune cells “home in to adhere” and finally extravasate into tissue. To understand the signaling cues that drive recruitment and adherence, my lab is focused on understanding the endothelial machinery with mechanotransduction (sensing alteration in blood flow) and chemotransduction (sensing chemical cues such as cigarette smoke, oxidants, endotoxins etc.) that upon activation initiates the immune response.

A major driver of amplification of inflammation is the NLRP3 inflammasome and we are currently engaged in studying its assembly using conventional in vitro and 3-D models of lungs and gingival tissue. Our goal is to block the redox signals that drive NLRP3 priming and activation to modulate and resolve the progression of inflammation in models of lung endothelium and in periodontal tissue.

The intersection of inflammation with disrupted circadian rhythm is also of interest to us. Alteration of circadian rhythm affects reactive oxygen species production and initiates redox signals in diverse cell types ranging from endothelium to osteoblasts and osteoclasts. In collaboration with researchers in sleep medicine, we are engaged in identifying the signaling pathways that are initiated upon sleep deprivation and that in turn activate signaling cascades associated with inflammation.

Laboratory Environment

• We are a racially and ethnically diverse group of individuals
• The lab environment is a welcoming and safe space to foster communication and empowerment