Grants and Contracts Details
Description
Abstract
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.
Status | Active |
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Effective start/end date | 9/17/21 → 8/31/26 |
Funding
- National Institute of Allergy and Infectious Diseases: $1,530,000.00
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