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Dr. Nilda Rodriguez

Dr. Nilda Rodriguez
Associate Professor
(319) 273-6505
McCollum Science Hall 85

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

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.

  1. Dixit UG, Rodríguez NE, Polando R, McDowell MA and Wilson ME (2021). "CR3 mediates ruffle-like, actin-rich aggregates during phagocytosis of Leishmania infantum metacyclics". Exp Parasitol 2021 Jan;220:107968  
  2. Lockard RD, Wilson ME and Rodríguez NE (2019). "Sex-related differences in immune response and symptomatic manifestations to infection with Leishmania species". J Immunol. Res., 2019, 1-14.
  3. Rodríguez NE, Lima DI, Dixit Gaur U, Turcotte EA, Lockard RD, Batra-Sharma H, Nascimiento EL, Jeronimo SMB and Wilson ME (2018). "Epidemiological and experimental evidence for sex-dependent differences in the outcome of Leishmania infantum infection". Am J Trop Med Hyg, 98, 142-145. 
  4. Rodríguez NE, Lockard RD, Turcotte EA, Araújo-Santos T, Bozza PT, Borges VM and Wilson ME (2017). "Lipid bodies accumulation in Leishmania infantum-infected C57BL/6 macrophages". Parasite Immunol. 2017;e12443. 
  5. Araújo-Santos T, Rodríguez NE, de Moura Pontes S, Dixit UG, Abánades DR, Bozza PT, Wilson ME and Matos-Borges V (2014). "Prostaglandin F2-alpha production in lipid bodies from Leishmania infantum chagasi is a critical virulence factor". J Infect Dis 210-1951-61.
  6. Rodríguez NE and Wilson ME (2014). "Eosinophils and mast cells in leishmaniasis". Immunol Res, 59, 129-141.
  7. Machado FS, Rodríguez NE (2/14) ...Tanowitz HB (2012). "Recent Developments in the interactions between caveolin and pathogens. Advances in Experimental Medicine and Biology 729:65-82
  8. Rodríguez NE, Dixit UG, Allen L-AH and Wilson ME (2011). "Stage-specific pathways of Leishmania infantum chagasi entry and phagosome maturation in macrophages". PLoS One 6, e19000. PMID:21552562
  9. Ueno N, Bratt CL, Rodríguez NE, and Wilson ME (2009). "Differences in human macrophage receptor usage, lysosomal fusion kinetics and survival between logarithmic and metacyclic Leishmania infantum chagasi promastigotes". Cell Microbiol 11, 1827-1841.
  10. Rodríguez NE, Gaur U, and Wilson, ME (2006). "Role of caveolae in Leishmania chagasi phagocytosis and intracellular survival in macrophages". Cell Microbiol 8, 1106-1120. **Chosen as cover illustration for this volume.**
  11. Rodríguez NE, Chang HK and Wilson ME (2004). "Novel program of macrophage gene expression induced by phagocytosis of Leishmania chagasi". Infect Immun 72, 2111-2122.
  12. Gantt KR, Schultz-Cherry S, Rodríguez NE, Jeronimo SM, Nascimento ET, Goldman TL, Recker TJ, Miller MA and Wilson ME (2003). "Activation of TGF-beta by Leishmania chagasi: importance for parasite survival in macrophages". J Immunol 170, 2613-2620.
  13. Wilson ME, Recker TJ, Rodríguez NE, Young BM, Burnell KK, Streit JA and Kline JN (2002). "The TGF-beta response to Leishmania chagasi in the absence of IL-12". Eur J Immunol 32, 3556-3565.
  14. Rauch DA, Rodríguez N and Roller RJ (2000). "Mutations in herpes simplex virus glycoprotein D distinguish entry of free virus from cell-cell spread". J Virol 74, 11437-11446.