down arrowMenu



                  Where life begins...

Dr. Nilda Rodriguez

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

Post-doctoral Training: 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: 
Cell Biology, Immunology, Microbiology

My 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.

  1. 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.
  2. 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.
  3. Rodríguez NE and Wilson ME (2014). "Eosinophils and Mast Cells in Leishmaniasis". Immunol Res, 59, 129-141.
  4. Rodríguez NE, Dixit UG, Allen, L-AH., and Wilson M.E. (2011). "Stage-Specific Pathways of Leishmania infantum chagasi Entry and Phagosome Maturation in Macrophages". PLoS One 6, e19000. PMID:21552562
  5. Machado FS, Rodríguez NE (2/14) ...Tanowitz HB. (2010). "Recent Developments in the Interactions between Caveolin and Pathogens. Chapter in the book: Caveolins and Caveolae: Roles in Signaling and Disease Mechanisms", P.G.F.a.M.P.L. Jean-Francois Jasmin, ed. (Landes Bioscience and Springer Science).
  6. 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.
  7. 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.**
  8. 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.
  9. Gantt KR, Schultz-Cherry S., Rodríguez N, 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.
  10. 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.
  11. 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.