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Secretion of Extracellular Vesicles from Babesia microti-infected Erythrocytes: Biological Roles in Host Macrophage Activation

Profile of female scientist wearing safety goggles, lab coat, and gloves looking at sample in test tube, two scientist in background.

ASTMH 2021 Annual Meeting

Virtual Event

November 18, 2021


Babesia microti is the primary cause of human babesiosis in North America. Despite recent increases in the disease, the pathogenesis and immune response to B. microti infection remain poorly understood. Studies in laboratory mice have shown a critical role for macrophages in eliminating parasites and parasitized red blood cells (RBCs). Notably, the effector parasite molecules that activate macrophages are still unknown. Recent evidence identified a novel protein export mechanism in B. microti that features a network of tubes of vesicles that extend from the parasite plasma membrane to the RBC cytoplasm. Vesicles harboring Babesia proteins are released from the infected RBC (iRBC) to the extracellular environment. We postulate that these parasite-derived extracellular vesicles (EVs) participate in intercellular communication between iRBCs and neighboring cells. When macrophages function as recipients, changes in the production of cytokines with key roles in the host innate immune response occur. To test this hypothesis, we examined cytokine responses in macrophages exposed to B. microti-iRBCs using an in vitro co-culture model. Pro-inflammatory cytokines such as IP-10, G-CSF, IL-6, TNF-α, MIP-1α, MIP-2, IL-1rα, and RANTES were markedly increased in the supernatants of macrophages co-incubated with iRBCs, as compared to uninfected RBCs, using antibody arrays. These effects were dependent on parasite growth, as treatment with the antiparasitic drug clindamycin resulted in significant decreases in cytokine secretion by macrophages exposed to iRBCs. These results support the hypothesis that soluble factors released by B. microti-iRBCs cause phenotypic changes in macrophages. Identification of secreted parasite antigens found in EVs isolated from iRBCs will provide insights into the mechanisms of intercellular communication between B. microti and macrophages that contribute to the induction of the innate immune response in the mammalian host. 

Download the poster to explore the secretion of extracellular vesicles from Babesia microti-infected erythrocytes.



Robert Molestina, headshot.

Robert Molestina, PhD

Lead Scientist, ATCC

Robert Molestina, PhD, is a Lead Scientist at ATCC. He has a background in scientific research in infectious diseases and execution of government-funded programs. Dr. Molestina serves as the subject matter expert in research and development activities in the Protistology and Malaria Laboratories which include, among others, the development of assays for molecular authentication of parasites, optimization of culture and cryopreservation protocols, and implementation of animal models for parasite propagation. In addition to managing parasitic protozoa and malaria resources under the BEI program, Dr. Molestina serves as the point of contact for arthropod vector resources offered through the BEI repository. His publication record for the last 20 years covers a diversity of scientific interests, including bacterial pathogenesis, molecular parasitology, eukaryotic microbiology, and proteomics of infectious disease.

Biniam Hagos, headshot

Biniam Hagos, MS

Lead Biologist, BEI Resources

Female, Aedes aegypti mosquito, from a left lateral perspective, while she was in the process of acquiring a blood meal from her human host

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