Dr. Nilda Rodriguez

Associate Professor

Dr. Nilda Rodriguez

Office - MSH 085

Research Lab - MSH 008

(319) 273-6505

Dr. Nilda Rodriguez

Associate Professor

  • Post-doctoral Training in Infectious Diseases: The University of Iowa and the VA Medical Center, Iowa City, IA
  • PhD in Microbiology: The University of Iowa
  • BS in Microbiology:  University of Puerto Rico
Teaching Interests

Microbiology, Cell Biology, Immunology

Research Interests

Our lab studies how the interactions between microbes and their hosts affect individual cells, the immune response, and ultimately, the outcome of infection. To examine these questions, we use a model of macrophage infection with Leishmania infantum. Leishmania spp. are parasitic protozoa endemic in over 90 tropical and subtropical countries. The World Health Organization (WHO) estimates that around 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".

Leishmaniasis is a vector-borne disease. The parasites are inoculated into the skin by the bite of infected sand flies. Parasites are then internalized by macrophages which are among the earliest immune cells to respond to infection. Inside the macrophages, Leishmania replicate, disseminate to new cells, and cause disease (CDC link).  Leishmania are remarkable in that they live and replicate inside macrophages, which are equipped to destroy pathogens. Hence, our studies are aimed to understand how this microbe can withstand the macrophage immune response. Our data showed that L. infantum resists macrophage attacks through a combination of several mechanisms including: 

 #1. Differently affecting the immune response of males and females.

 #2. Modulating the inflammatory and anti-inflammatory molecules of macrophages.

 #3. Virulence- and stage-dependent parasite entry and intracellular trafficking.

We hypothesize that molecular differences in cells derived from males versus females in combination with parasite virulence factors result in differential uptake, intracellular trafficking, and macrophage signaling leading to distinct outcomes of infection. Future work in our lab will include examination of how the immune response to Leishmania infection differs between cells of male- versus female-origin. In addition, using fluorescence microscopy, we will examine entry and intracellular trafficking pathways used by the parasite to initiate and propagate infection. Altogether, the goal of this lab is to contribute to the understanding of the cellular processes involved in the immune response to intracellular pathogens.

Professional Accomplishments