Specific expression of FABP5 in type II alveolar epithelial cells in silicosis pulmonary fibrosis based on single-cell transcriptome sequencing

Background Silicosis is caused by long-term inhalation of large amounts of free silica (SiO₂) particles, and exploring its mechanism can provide new directions for the treatment of silicosis fibrosis.

Objective To investigate the expression and role of fatty acid binding protein 5 (FABP5) in a silica-induced silicosis model.

Methods In combination with the results of single-cell transcriptome sequencing, the expression pattern of FABP5 in mouse alveolar epithelial cells was explored by bioinformatic analysis, and the distribution pattern of fabp5 was detected by spatial transcriptomics. An in vivo model of silicosis was established by intratracheal injection with SiO₂ into mice and four groups were set up: normal saline (NS) 7 d group, NS 56 d group, SiO₂ 7 d group, and SiO₂ 56 d group. An in vitro model of silicosis was established in SiO₂-treated mouse lung epithelial cell line (MLE-12). At the whole animal level, the marker of epithelial cells (E-Cad) and the protein level of FABP5 were detected by tissue immunofluorescence assay; in vitro, the changes of fabp5 mRNA expression and protein level in MLE-12.

Results The results of single-cell transcriptome sequencing and spatial transcriptome sequencing showed that the mRNA expression of fabp5 was upregulated in type II alveolar epithelial cells in the focal area of silicosis in mice, accompanied by elevated tissue immunofluorescent protein levels, and there was co-localization of E-CAD. Meanwhile, SiO₂ stimulation induced a 1.58-fold increase in fabp5 mRNA expression and a 2-fold increase in protein levels in MLE-12 cells, with significant differences (P<0.05).

Conclusion The protein level of FABP5 is increased in alveolar epithelial cells in a pulmonary fibrosis model, suggesting that FABP5 may be involved in the pathological process of epithelial cells in pulmonary fibrosis.