Apoptotic bodies derived from hypoxic bone marrow mesenchymal stem cells reverse LPS-induced apoptosis delay in neutrophils.

ABSTRACT: Immune system disorders underlie numerous chronic inflammatory diseases. Functional status and normal apoptosis of neutrophils are of great significance in the regulation and outcome of inflammation. Excessive activation and delayed apoptosis of neutrophils can lead to additional tissue damage, which may be an important cause of delayed disease recovery. Stem cells have immunomodulatory effects, but transplanted stem cells are prone to apoptosis in the hypoxic-inflammatory microenvironment. However, the capacity of stem cell-derived apoptotic bodies (ApoBDs) to regulate neutrophil functions, along with the specific components and mechanisms involved, is still unclear. Our study revealed that ApoBDs stemming from hypoxia-induced apoptosis in bone marrow mesenchymal stem cells reversed Lipop

SUBMITTER: Zhao Y 

PROVIDER: S-EPMC12530883 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature