An opsonic peptide promotes radiation-induced macrophage extracellular trap clearance to alleviate inflammation
- 1Center for Immunology and Inflammation, The Feinstein Institutes for Medical Research
- 2Departments of Surgery and Molecular Medicine, Zucker School of Medicine at Hofstra/Northwell
Abstract
Ionizing radiation exposure leads to inflammation and tissue damage, in which macrophage extracellular traps (METs) may play a role. Effective strategies to mitigate inflammation caused by radiation-induced METs are needed. We have recently developed a novel opsonic peptide, OP18, that targets multiple damage-associated molecular patterns (DAMPs) and enhances their clearance by macrophages. Because METs contain DAMPs, including histone H3 and high-mobility group box 1 protein (HMGB1), we hypothesize that OP18 promotes the clearance of radiation-induced METs and thereby reduces inflammation. In vitro studies were conducted using macrophages exposed to radiation and METs, with or without OP18 treatment. METs uptake, endo-lysosomal trafficking, integrin involvement, mitochondrial function, NF-κB activation, and cytokine release were assessed. OP18 significantly enhances MET uptake by macrophages, an effect that is mediated by α v β ₃ -integrin and involves the endo-lysosomal trafficking. This enhanced clearance by OP18 alleviates METs-induced mitochondrial stress and restores metabolic function (ATP production, basal/maximal respiration) in macrophages. Furthermore, OP18 treatment exhibits a trend towards decreasing METs-induced NF-κB activation while increasing the release of anti-inflammatory cytokine IL-10. OP18 represents a novel therapeutic approach to mitigate radiation-induced inflammation by promoting the efficient clearance of pro-inflammatory METs, thereby restoring cellular homeostasis and dampening inflammatory signaling.
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BibTeX
@article{lee2026opsonic,
title = {{An opsonic peptide promotes radiation-induced macrophage extracellular trap clearance to alleviate inflammation}},
author = {Yongchan Lee and Gaifeng Ma and Dilara Aylar and Monowar Aziz and Ping Wang},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1970645},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1970645/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - An opsonic peptide promotes radiation-induced macrophage extracellular trap clearance to alleviate inflammation
AU - Yongchan Lee
AU - Gaifeng Ma
AU - Dilara Aylar
AU - Monowar Aziz
AU - Ping Wang
PY - 2026
DA - 2026/10/12
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1970645
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1970645/full
AB - Ionizing radiation exposure leads to inflammation and tissue damage, in which macrophage extracellular traps (METs) may play a role. Effective strategies to mitigate inflammation caused by radiation-induced METs are needed. We have recently developed a novel opsonic peptide, OP18, that targets multiple damage-associated molecular patterns (DAMPs) and enhances their clearance by macrophages. Because METs contain DAMPs, including histone H3 and high-mobility group box 1 protein (HMGB1), we hypothesize that OP18 promotes the clearance of radiation-induced METs and thereby reduces inflammation. In vitro studies were conducted using macrophages exposed to radiation and METs, with or without OP18 treatment. METs uptake, endo-lysosomal trafficking, integrin involvement, mitochondrial function, NF-κB activation, and cytokine release were assessed. OP18 significantly enhances MET uptake by macrophages, an effect that is mediated by α v β ₃ -integrin and involves the endo-lysosomal trafficking. This enhanced clearance by OP18 alleviates METs-induced mitochondrial stress and restores metabolic function (ATP production, basal/maximal respiration) in macrophages. Furthermore, OP18 treatment exhibits a trend towards decreasing METs-induced NF-κB activation while increasing the release of anti-inflammatory cytokine IL-10. OP18 represents a novel therapeutic approach to mitigate radiation-induced inflammation by promoting the efficient clearance of pro-inflammatory METs, thereby restoring cellular homeostasis and dampening inflammatory signaling.
SN - 1664-3224
ER -