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

ABSTRACT:

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.

Meth

SUBMITTER: Ma X 

PROVIDER: S-EPMC7066891 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature