# HDAC6 regulation of myeloid cell responses in sepsis

> **NIH NIH R01** · UNIVERSITY OF KENTUCKY · 2024 · $382,500

## Abstract

Project Summary
Sepsis is a life-threatening disease caused by dysregulated host responses to infection. Sepsis
remains a major health problem worldwide with high mortality. Myeloid cell responses such as
endotoxin tolerance, epigenetic modification, metabolic failure, and apoptosis are profoundly
affected in sepsis, which leads to systemic dysfunction of immune cells and progenitor cells. The
regulation of myeloid cell responses in sepsis remains largely unknown. The histone deacetylase
HDAC6 regulates a variety of cellular responses. However, HDAC6 regulation of myeloid cell
responses in sepsis has not been investigated. Our preliminary studies indicate that HDAC6 is a
key mediator of cell signaling in myeloid cells. Myeloid-specific HDAC6 deletion reduces the
mortality in septic mice. Furthermore, selective HDAC6 inhibition can modulate myeloid cell
responses in the mouse models of sepsis. In the proposed studies, we will test the hypothesis
that HDAC6 activation mediates myeloid cell dysfunction in sepsis, and HDAC6 inhibition could
improve myeloid cell function and survival rate in sepsis.

## Key facts

- **NIH application ID:** 10896154
- **Project number:** 5R01AI167297-04
- **Recipient organization:** UNIVERSITY OF KENTUCKY
- **Principal Investigator:** Jian Fu
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $382,500
- **Award type:** 5
- **Project period:** 2021-09-17 → 2026-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10896154

## Citation

> US National Institutes of Health, RePORTER application 10896154, HDAC6 regulation of myeloid cell responses in sepsis (5R01AI167297-04). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10896154. Licensed CC0.

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