Dr. Melehani completed his medical and graduate research training at the University of North Carolina, Chapel Hill, earning both a medical degree and a doctorate in pharmacology. In his dissertation research, Dr. Melehani studied the molecular mechanism by which the innate immune system and Staphylococcus aureus interact. During his time in graduate and medical school, Dr. Melehani developed an interest in drug development - understanding the evidence supporting our use of medications in the clinic, as well as the process of discovering new targets and creating new medicines. To better understand this process, Dr. Melehani worked as a fellow at Hatteras Venture Partners, a healthcare- and biotechnology-focused venture capital firm in North Carolina. At Hatteras, Dr. Melehani worked closely with the investment team and managing partners to evaluate early-stage therapeutic development companies to find those with the greatest potential for transforming medicine.
Now, at Stanford, Dr. Melehani is a resident in the Internal Medicine program and a member of the Translational Investigator Program. He has an interest in smoking-related lung diseases and immune-mediated pathogenesis in lung disease. As such, he has a clinical interest in Pulmonary Medicine and Rheumatology. His goal is to develop an expertise in understanding the role of the immune system in lung diseases from chronic obstructive pulmonary disease (COPD) to connective tissue disease-associated interstitial lung diseases (CTD-ILD) with a specific focus on how smoking leads to immune dysfunction and disease. He hopes to develop a research program focused on developing novel therapies for these indications.
Toxoplasma Co-opts Host Cells It Does Not Invade
2012; 8 (7)
Like many intracellular microbes, the protozoan parasite Toxoplasma gondii injects effector proteins into cells it invades. One group of these effector proteins is injected from specialized organelles called the rhoptries, which have previously been described to discharge their contents only during successful invasion of a host cell. In this report, using several reporter systems, we show that in vitro the parasite injects rhoptry proteins into cells it does not productively invade and that the rhoptry effector proteins can manipulate the uninfected cell in a similar manner to infected cells. In addition, as one of the reporter systems uses a rhoptry:Cre recombinase fusion protein, we show that in Cre-reporter mice infected with an encysting Toxoplasma-Cre strain, uninfected-injected cells, which could be derived from aborted invasion or cell-intrinsic killing after invasion, are actually more common than infected-injected cells, especially in the mouse brain, where Toxoplasma encysts and persists. This phenomenon has important implications for how Toxoplasma globally affects its host and opens a new avenue for how other intracellular microbes may similarly manipulate the host environment at large.
View details for DOI 10.1371/journal.ppat.1002825
View details for Web of Science ID 000306837700043
View details for PubMedID 22910631
View details for PubMedCentralID PMC3406079