# Neutrophil migration and inflammation

> **NIH NIH R35** · PURDUE UNIVERSITY · 2022 · $419,512

## Abstract

Inflammation presents as swelling, redness, heat, and lost-of-function and is essential for the restoration of
tissue homeostasis after injury and infection. Neutrophils are the major effector cells of acute inflammation that
combat infection, promote wound healing and resolution of inflammation, while contributing to collateral tissue
injury. In addition, neutrophils are exploited as vehicles that cross tissue barriers to deliver cargos to
inflammation sites. A better understanding of the neutrophil-intrinsic mechanisms that regulate neutrophil
migration will have broad translational importance in the prevention and treatment of a wide range of
inflammation-related diseases. The challenges associated with studying neutrophils are a limited set of genetic
tools and the plasticity of the cells in vivo. To address these challenges, the PI uses zebrafish, a genetically
tractable vertebrate model with a well-conserved innate immune system. Findings on neutrophil intrinsic genes
that regulate neutrophil migration generated in the zebrafish model are then validated in primary human or
murine neutrophils. MicroRNAs are small RNA molecules of 22-24 nt that regulate homeostasis in health and
disease. MicroRNA “mimics” and “inhibitors” are emerging as next-generation therapeutics because of their
ability to modulate a network of genes. In addition, microRNAs are being used as tools to discover novel
regulators of biological processes. A critical gap remains understanding how microRNAs regulate neutrophil
function: despite the prominent microRNA profiling studies in neutrophils and in various diseases, microRNA
functional studies are scarce. The PI’s lab has been at the forefront of addressing this unmet need by
characterizing microRNAs and their targets in neutrophil migration. Building on their recent progress, the first
project is to continue charactering microRNAs in regulating neutrophil migration with two sub aims: (1.1)
identify microRNA targets as novel regulators of neutrophil migration and inflammation, and (1.2) characterize
how RORα regulates neutrophil migration. A separate project is to characterize mechanisms delineating the
role of mitochondria in neutrophil migration. Mitochondria fission promotes migration in many cell types,
including lymphocytes, presumably by increasing mitochondria localization and ATP production at sites of high
energy demand. On contrary, neutrophils possess a highly fused mitochondrial network and primarily use
glycolysis for ATP generation, suggesting additional roles of mitochondria outside the realm of ATP.
Specifically, the PI seeks to (2.1) characterize how MFN2 regulates neutrophil migration. The hypothesis is that
MFN2-mediated mitochondrial-ER contact regulates Rac activation and neutrophil adhesion and migration.
The PI will continue to (2.2) identify additional mitochondrial related genes as novel regulators of neutrophil
migration and inflammation. An increased understanding of neutrophil migration and in...

## Key facts

- **NIH application ID:** 10427294
- **Project number:** 5R35GM119787-07
- **Recipient organization:** PURDUE UNIVERSITY
- **Principal Investigator:** Qing Deng
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $419,512
- **Award type:** 5
- **Project period:** 2016-08-11 → 2026-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10427294

## Citation

> US National Institutes of Health, RePORTER application 10427294, Neutrophil migration and inflammation (5R35GM119787-07). Retrieved via AI Analytics 2026-05-21 from https://api.ai-analytics.org/grant/nih/10427294. Licensed CC0.

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