Dr. Kailash Gulshan, an assistant professor in the Department of Biology, Geology, and Environmental Science (BGES) and a member of the Center for Gene Regulation in Health and Disease (GRHD), and his team (pictured right) published two papers in iScience, a high impact journal from Cell Press. Dr. Gulshan's laboratory studies a protein called Gasdermin D (GsdmD), which forms pores in cellular membrane to release inflammatory molecules from macrophages and other immune cells. The published works highlight the pivotal role of inflammation control in lung cancer and atherosclerosis. Dr. C. Alicia Traughber, Postdoctoral Fellow, is the first author in both papers. Other members of the research team are CSU graduate students Mariam Khan, Kalash Neupane, and Nilam Bhandari, and postdoctoral fellow Dr. Ashutosh Prince, as well as several collaborators from the Cleveland Clinic's Lerner Research Institute.

In the first study the team found a novel role of GsdmD in lung cancer. As the cancer progresses, immune cells such as macrophages are recruited to the tumor area. In some cases, these tumor-associated macrophages, instead of killing cancer cells, undergo pyroptotic cell death and release inflammatory molecules through GsdmD pores. As result, the immune system is suppressed and cancer cells are able to evade the immune system. Moreover, the immune cells create a tumor microenvironment, which is more suitable for cancerous growth. This vicious cycle can be interrupted by deletion of GsdmD, which suggest that GsdmD is a potential target for pharmacological intervention in lung cancer.

In the second study, Dr. Gulshan's team found that Miltefosine, a broad-spectrum antimicrobial agent developed in 1980 and approved by FDA to treat the parasitic disease Leishmaniasis, can also protect against atherosclerosis. It was previously known that Miltefosine induces cholesterol efflux from cells. The study uncovered that Miltefosine can also control inflammation. Treatment with Miltefosine blocks the formation of GsdmD pores and the release inflammatory molecules, which reduces artery plaque formation and growth.