Dr. Nilda Rodriguez has received his PhD in The University of Iowa currently, she is working as AssistantProfessor in University of Northern Iowa.  

Dr. Nilda Rodriguez research studies how the early interactions between microbes and their hosts affect individual cells, the immune response, and ultimately, the outcome of infection. To examine these questions, I study the interactions between Leishmania infantum chagasi (Lic) and macrophages of mouse origin. Leishmania spp. are parasitic protozoa endemic in 90 tropical and subtropical countries. The World Health Organization (WHO) estimates that 350 million people are at risk of Leishmania infection, making it a major threat to global health. Unfortunately, because most people at risk live in developing countries, little effort has been given to find effective treatments, leading the WHO to classify Leishmaniasis as a "neglected disease". Leishmania spp. have a life cycle consisting of an initial stage, the promastigote, and a replicative stage, the amastigote. The promastigote is inoculated by the sand fly vector into the mammalian host during a blood meal, whereupon it is internalized by macrophages. Inside the macrophage, the parasite converts into the amastigote form, which has the ability to replicate, disseminate to new macrophages and cause disease. Leishmania spp. are remarkable in that they survive and thrive inside macrophages, which are immune cells equipped to destroy pathogens. Hence, our studies are aimed to study how Lic is able to survive the hostile environment of the macrophage. Our data showed that Lic resists macrophage attack through a combination of several mechanisms including: #1. Modulation of macrophage molecules involved in inflammatory and anti-inflammatory responses. #2. Entry through cholesterol-rich microdomains on the macrophage surface. #3. Differential intracellular trafficking in macrophages. These results have led us to hypothesize that the mechanisms of microbial uptake set the stage for the pathways of pathogen intracellular traffic as well as the signaling cascades that control the macrophage response to infection. Future work in our lab will include examination of the entry and intracellular trafficking pathways used by promastigotes and amastigotes to initiate and propagate infection, respectively. Examination of parasite intracellular trafficking will involve the use of fluorescence microscopy. Additional experiments will include investigation of the role of cholesterol-rich microdomains in the ability of macrophages to elicit an effective immune response. All together, the ultimate goal of this lab will be to develop a research program that contributes to the understanding of the cellular processes modulating the macrophage response to intracellular pathogens.