Inflammatory and immune-related factor Caspase 1 contributes to the development of oral lichen planus

In this study, we aimed at underlying the potential regulatory mechanism and overall biological functions of caspase 1 (CASP1) in oral lichen planus (OLP).

Buccal mucosa tissue samples were gained from healthy subjects or patients diagnosed with OLP. Immunochemical staining was applied to detect CASP1 in OLP tissues. Lipopolysaccharide (LPS) was used to construct OLP in vitro models. Cell counting kit-8 (CCK-8) and flow cytometry assay were applied to detecte cell viability and apoptosis.

The upregulation of CASP1 in OLP has been identified through comprehensive bioinformatics analysis and verified in clinical samples. In OLP tissues, inflammation-related factors, including tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, and IL-18, were elevated and positively correlated with CASP1. In HaCaT cells, LPS stimulation induced CASP1 upregulation, suppressed cell viability, facilitated cell apoptosis, and elevated the levels of TNF-α, IL-1β, IL-6, and IL-18; silencing of CASP1 attenuated LPS-induced damages to HaCaT cells. Pearson's correlation analysis identified that 45 immune-related genes were positively correlated with CASP1; these 45 genes were enriched in the immune system process, associated with combined immunodeficiency, and spleen-specific and CD56 + NK cell-specific. PPI network among CASP1 and correlated immune-related factors was constructed, and CASP1 was positively correlated with RAC2, CYBB, and ARHGDIB. In HaCaT cells, LPS stimulation induced RAC2, CYBB, and ARHGDIB expression, whereas knocking down CASP1 attenuated LPS-induced increases in RAC2, CYBB, and ARHGDIB.

CASP1 is upregulated in OLP tissues. Knockdown of CASP1 in HaCaT cells could protect HaCaT cells from LPS-induced inflammatory injury. Comprehensive bioinformatics indicates that the interaction of CASP1 with RAC2, CYBB, and ARHGDIB, might be the potential molecular mechanism.