The IL1β-HER2-CLDN18/CLDN4 axis mediates lung barrier damage in ARDS.

OBJECTIVE

The high mortality rate associated with acute respiratory distress syndrome (ARDS) is a major challenge for intensive care units. In the present study, we applied bioinformatics and animal models to identify core genes and potential corresponding pathways in ARDS.

RESULTS

Using bioinformatics analysis, IL-1β was identified as the core gene of ARDS. Cell experiments showed that up-regulation of IL-1β downregulates claudin18 to promote lung barrier function damage by regulating the IL-1β-HER2/HER3 axis, further promoting the development of ARDS. This was validated in the animal models.

CONCLUSION

IL-1β promotes the development of ARDS by regulating the IL-1β-HER2/HER3 axis. These findings deepen the understanding of the pathological mechanisms of ARDS.

METHODS

Transcription data sets related to ARDS were subjected to differential expression gene analysis, functional enrichment analysis, and receiver operating characteristic curve analysis and, so as to identify core genes in ARDS. Cell experiments were used to further explore the effects of core genes on lung barrier function damage. Animal models were applied to validate the effects of core gene in mediating biological signal pathways in ARDS.