Parasitic helminths can live in their hosts for decades and have potent immunosuppressive mechanisms that can prevent their rejection by the immune system. These immunosuppressive mechanisms are also the basis of some aspects of the 'hygiene hypothesis'; suggesting that worm infection may protect their hosts from inflammatory bowel diseases and reduce the severity of colitis. We are hoping to better understand the immunoregulatory mechanisms by which helminth infection could suppress mucosal responses in the gastrointestinal tract.
Looking into M2 macrophages that we know are critical for enabling the host to tolerate and resist helminth infections, we are now hoping to characterize the origin and functional properties of these macrophages in different inflammatory diseases. One specific inflammatory disorder is atherosclerosis: a leading cause of death worldwide. It is widely known that heart disease progression and regression have been associated with different activation levels of macrophages inside aortic plaque. We are hoping through our experiments to better characterize these activation states and in turn identify a possible therapeutic target.