# Inflammation-associated anemia and the role of monocyte-derived inflammatory hemophagocytes in a model of blood-stage malaria

> **NIH NIH F32** · BENAROYA RESEARCH INST AT VIRGINIA MASON · 2020 · $65,310

## Abstract

Project Summary/Abstract
Malaria is caused by protozoan parasites of the Plasmodium species and is a major health problem within
malaria-endemic regions. Disease symptoms range from mild to severe, and severe malaria is associated with
a variety of complications, including severe malarial anemia. Malarial anemia can be life-threatening, especially
in the most vulnerable groups - young children and pregnant women. The mechanisms leading to malarial
anemia are not well understood, although dysregulated immune responses have been implicated. Our group
recently identified a unique population of inflammatory hemophagocytes that develop in response to
Plasmodium yoelii 17XNL infection, a nonlethal model of blood stage malaria. The development of these
inflammatory hemophagocytes (iHPCs) correlates with anemia and thrombocytopenia, although the
mechanisms leading to the development of this novel cell type and its contributions, both direct and indirect, to
malarial anemia have yet to be explored. This application aims to investigate the role of iHPCs in the
development of malarial anemia during Plasmodium infection. The central hypothesis of this research proposal
is that iHPCs differentiate from monocytes in response to cell-intrinsic signaling through Toll-like receptors
during infection, and that these cells are responsible for the development of malarial anemia through
hemophagocytosis. This application seeks to better understand the signaling and cell types necessary for
iHPC development during Plasmodium infection (Aim 1), including the signals and receptors that license iHPCs
to consume red blood cells and platelets under inflammatory conditions (Aim 2). Additionally, we will assess
whether Plasmodium- infected individuals in malaria-endemic regions develop iHPCs during febrile illness, and
whether these cells correlate with the development of anemia (Aim 3). The proposed research will result in a
better understanding of the mechanisms leading to malarial anemia, and has the potential to elucidate possible
intervention strategies or therapeutic targets that could reduce illness and mortality during malarial anemia.
The completion of experiments outlined in this application under the guidance of Dr. Jessica Hamerman, along
with the training plan described in the supporting documents, are key steps toward my goal of becoming an
independent scientist. At the completion of this fellowship, I will be prepared to begin my own laboratory as an
independent academic investigator.

## Key facts

- **NIH application ID:** 10069131
- **Project number:** 1F32HL154700-01
- **Recipient organization:** BENAROYA RESEARCH INST AT VIRGINIA MASON
- **Principal Investigator:** Susana Lucia Orozco
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $65,310
- **Award type:** 1
- **Project period:** 2020-08-01 → 2023-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10069131

## Citation

> US National Institutes of Health, RePORTER application 10069131, Inflammation-associated anemia and the role of monocyte-derived inflammatory hemophagocytes in a model of blood-stage malaria (1F32HL154700-01). Retrieved via AI Analytics 2026-05-21 from https://api.ai-analytics.org/grant/nih/10069131. Licensed CC0.

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