The pathogenesis of Acute Exogenous Lipid Pneumonia based on proteomics

Abstract

Introduction Acute exogenous lipoid pneumonia (AELP) is a rare disease. At present, the specific pathogenesis of AELP is unclear, and there is no safe and effective specific drug. The purpose of this study is to explore the biological processes, signal pathways and key proteins involved in AELP through proteomics, bioinformatics and polymerase chain reaction, so as to deepen the study of the pathogenesis of AELP. Methods The experimental rats were randomly divided into 2 groups: experiment group (inhaled 0.5 ml/kg of sewing machine oil) and control group (inhaled 0.5 ml/kg of normal saline). Collect the proteins in the upper lobe of the right lung of mice for proteomic sequencing to obtain the expression data, use the differential analysis software MaxQuant to screen the differentially expressed proteins (DEPs), and use the bioinformatics analysis method to carry out gene ontology function (GO), Kyoto Encyclopedia of genes and genomes (KEGG) analysis and protein-protein interaction (PPI) network construction for DEGs, Eleven key proteins (PADI4, IGF2, SMPDL3B, UHRF1, ANXA8, DEFB4, F3, MK167, SLC39A4, LIMD1 and GJA1) were detected by Reverse-transcription polymerase chain reaction (RT-PCR) for validation. Results A total of 1253 DEPs were obtained after comparing the data of the experimental group and the control group with the proteome, including 843 up-regulated proteins and 410 down-regulated proteins. Through the functional analysis of GO and KEGG, it is found that these DEPs mainly participate in the regulation process of integrin binding, proteoglycan binding, chemokine receptor binding, receiver regulator binding, and cytokine activity, and are significantly enriched in proteoglycan binding and other signal pathways. PPI network construction was carried out for DEPs to screen out proteins with high correlation, such as ACTN3, CX3CR1, CCR3, AGT, MYLPF. 11 proteins were verified by RT-PCR，compared with the control group, 9 proteins (PADI4, IGF2, SMPDL3B, UHRF1, ANXA8, MK167, SLC39A4, LIMD1 and GJA1) were significantly up-regulated in the experimental group. Conclusion Our findings identified that PADI4, IGF2, UHRF1, DEFB4 and GJA1 proteins may be potential diagnostic biomarker of AELP.