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CLCF1/NF-κB signaling pathway regulates macrophage efferocytosis to ameliorate neurological damage and cognitive dysfunction following CO poisoning

ABSTRACT: Severe carbon monoxide (CO) poisoning can induce structural damage to the nervous system, leading to long-term cognitive dysfunction in patients. The proper termination of the inflammatory response caused by neuronal cell damage is a prerequisite for tissue repair. Macrophages can clear cell corpses/fragments caused by brain injury through efferocytosis and produce cytokines to coordinate immune responses, thereby promoting neuronal repair and regeneration. However, in the microenvironment of the nervous system affected by CO poisoning, the function of macrophages is inhibited. Our study found that CLCF1 can regulate the secretion of cytokines such as TNF-α, IL-1β, and IL-10 through the NF-κB signaling pathway, thereby affecting neuronal cell repair and regeneration.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE250190 | GEO | 2024/01/01

REPOSITORIES: GEO

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CLCF1/NF-κB Signaling Pathway Regulates Macrophage Efferocytosis to Ameliorate Neural Damage and Cognitive Dysfunction After CO Poisoning.

Project description:Severe carbon monoxide (CO) poisoning can cause structural damage to the nervous system, leading to long-term cognitive dysfunction in patients. Correctly terminating the inflammatory response caused by neuronal damage is a prerequisite for tissue repair. Macrophages can clear the cell corpses/fragments caused by brain injury through efferocytosis, and produce cytokines to coordinate the immune response, promoting neuronal repair and regeneration. However, in the microenvironment of the nervous system affected by CO poisoning, the function of macrophages is inhibited. Our research found that CLCF1 can regulate the secretion of cytokines such as TNF-α, IL-1β, and IL-10 through the NF-κB signaling pathway, thereby affecting neural cell repair and regeneration. Simultaneously, CLCF1 can regulate the efferocytosis function of macrophages, thus controlling the degree of inflammation and assisting in the repair of the damaged nervous system. In experiments, it was observed that targeting the regulation of macrophage CLCF1 expression led to improvements in memory, learning, and motor abilities in rats poisoned with CO.

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