The role of the STING inflammatory pathway in hepatic damage in psoriasis with type 2 diabetes mellitus

Introduction: Studies have suggested a potential association between patients who have both psoriasis and diabetes and liver damage. However, the exact nature of this link has not yet been fully established. The objective of the current study was to examine the potential exacerbation of liver damage due to the coexistence of psoriasis and type 2 diabetes mellitus (T2DM) and to explore the impact of interferon gene stimulating factor (STING) on related damage. Material and methods: Four patient groups were recruited: normal individuals, individuals with diabetes, those with psoriasis, and those with both diabetes and psoriasis. Relevant indicators were collected to facilitate the investigation. Furthermore, a mouse model of psoriasis combined with T2DM was established. The expression levels of STING and inflammatory factors downstream of the pathway were detected in both the skin and liver tissues of the model mice. Results: Based on our findings, patients with both psoriasis and T2DM exhibit abnormal liver function and increased STING expression in the skin (p < 0.05). In the in vivo experiments, liver tissues from model mice exhibited significantly elevated expression of STING and its downstream inflammatory factors, including NF-kappa B p65, interferon-beta, interleukin (IL)-17A, and IL-23 (p < 0.05). The STING inhibitor-treated group displayed reduced skin damage and improved liver histopathology (p < 0.05). Conclusions: The findings of the current study indicate that the STING inflammatory pathway is upregulated in the liver tissues of individuals with psoriasis and T2DM.