BioProject

Severe carbon monoxide (CO) poisoning can cause structural damage to the nervous system, leading to long-term cognitive dysfunction in patients. More...

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. Overall design: Rats were used to create an acute carbon monoxide (CO) poisoning model, following the method described by Li et al.[1]. The rats were placed in a sealed experimental chamber and initially inhaled CO gas with a concentration of 1000 ppm for 40 minutes; this was followed by inhalation of CO gas at a concentration of 3000 ppm for 20 minutes. The model was considered successful for acute severe CO poisoning if the rats exhibited symptoms of impaired consciousness accompanied by high carboxyhemoglobin (HbCO) concentrations (>60%). Brain tissue cell suspensions were extracted from three CO-poisoned rats and three normal control (NC) group rats for single-cell sequencing. Gel beads containing barcode sequences were mixed with the samples and combined with oil surfactants to form Gel Bead-In-Emulsions (GEMs). The GEMs were collected into a reservoir for constructing 10x single-cell transcriptome libraries. An Illumina NovaSeq PE150 sequencing strategy was employed, targeting 50,000-100,000 reads per cell, corresponding to 15-30M data points per cell. Each experimental group was repeated three times to verify the reliability of the results. The raw data were mapped to the Rnor_6.0 rat reference genome using CellRanger (10x Genomics). Less...