Inflammation: macrophage responses to pore-forming toxins
Inflammation is a crucial component of many diseases, regardless of whether they are caused by autoimmunity, pathogenic microbes, tumors, or even particles and chemicals. Inflammation is also necessary to develop robust responses to vaccines. This inflammation depends on the response of macrophages and other innate immune cells to pathogenic conditions.
The research in my lab aims to elucidate novel mechanisms of inflammation by studying the interplay and downstream effects of bacterial pore-forming toxins, which trigger inflammation, on macrophages. Streptolysin O is an archetypal pore-forming toxin that can directly lyse cells. Interestingly, macrophages can withstand high doses of toxin. At these sublytic concentrations, macrophages resist the damage and execute a pro-inflammatory pathway. Understanding what mechanisms are required for damage resistance will help us regulate the inflammatory response, as well as apply that knowledge to other diseases directly related to membrane damage, such as muscular dystrophies.
