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PSTPIP2 is associated with disease severity in patients with pressure ulcer sepsis and has anti-inflammatory effects
Xiaoxia Wang1, Youli Wang2, Jianjun Luo1
1Department of Critical Care Medicine, The 903rd Hospital of the Joint Logistics Support Force of the Chinese People's Liberation Army, Hangzhou, Zhejiang Province, China.
Background:
One of the common adverse reactions in patients with pressure ulcers (PU) is sepsis, which is mainly related to microbial infections caused by pathogenic organisms. The activation of nuclear factor kappa-B (NF-κB) frequently occurs in conjunction with pathogenic microbial infections. Proline-serine-threonine-phosphatase-interacting protein 2 (PSTPIP2) is closely related to inflammatory disorders. The role and mechanism of PSTPIP2 in sepsis because of pressure ulcers is unclear. In this study, we discovered that PSTPIP2 was lowly expressed in peripheral blood of patients with sepsis induced by pressure ulcers.
Methods:
Peripheral blood was collected from 20 patients with sepsis due to pressure ulcers and 10 healthy controls, and the expression of PSTPIP2 in peripheral blood was discovered by polymerase chain reaction and Western blot analysis. Information on the clinical characteristics of patients was summarized, and the expression data of PSTPIP2 were correlated with the patients' acute physiology and chronic health evaluation (APACHE) II score, sequential organ failure assessment (SOFA) score, and C-reactive protein (CRP) and procalcitonin (PCT) scores by Spearman's correlation analysis. One of the main mediators of Gram-negative sepsis is lipopolysaccharide (LPS). In order to establish an in vitro sepsis model, THP-1 cells were treated with LPS, and the cells were transfected with PSTPIP2. Contents of interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor-α (TNF-α) in each group of cells were detected by enzyme-linked--immunosorbent serologic assay, and NF-κB-related proteins were detected by Western blot analysis.
Results:
When compared to healthy controls, the peripheral blood of patients with pressure sepsis had lower PSTPIP2 expression, which had a negative correlation with the APACHE II, SOFA, CRP, and PCT scores. LPS-induced THP-1 cells expressed less PSTPIP2 than the untreated control cells, and PSTPIP2 transfection decreased IL-6, IL-1β, and TNF-α levels and inhibited the activation of NF-κB pathway.
Conclusion:
PSTPIP2 is associated with disease severity in patients with pressure ulcer sepsis and has anti-inflammatory effects.
Insights
Proline-serine-threonine-phosphatase-interacting protein 2 (PSTPIP2) is expressed at lower levels in patients with pressure ulcer sepsis. Lower PSTPIP2 expression correlates with increased disease severity and exhibits anti-inflammatory effects.
Area of Science:
- Biomedical Science
- Immunology
- Molecular Biology
Background:
- Sepsis from pressure ulcers is a common adverse event linked to microbial infections.
- Nuclear factor kappa-B (NF-κB) activation is often observed in microbial infections.
- Proline-serine-threonine-phosphatase-interacting protein 2 (PSTPIP2) is implicated in inflammatory disorders, but its role in pressure ulcer sepsis is unknown.
Purpose of the Study:
- To investigate the expression and role of PSTPIP2 in sepsis induced by pressure ulcers.
- To determine the correlation between PSTPIP2 expression and disease severity markers.
- To elucidate the anti-inflammatory mechanisms of PSTPIP2 in a sepsis model.
Main Methods:
- Peripheral blood samples were analyzed for PSTPIP2 expression in patients with pressure ulcer sepsis and healthy controls using PCR and Western blot.
- Spearman's correlation analysis was used to assess the relationship between PSTPIP2 expression and clinical scores (APACHE II, SOFA) and inflammatory markers (CRP, PCT).
- An in vitro sepsis model using THP-1 cells treated with lipopolysaccharide (LPS) was established to study PSTPIP2's effects on inflammatory cytokine production (IL-6, IL-1β, TNF-α) and NF-κB pathway activation.
Main Results:
- PSTPIP2 expression was significantly lower in patients with pressure ulcer sepsis compared to healthy controls.
- Reduced PSTPIP2 levels negatively correlated with APACHE II, SOFA, CRP, and PCT scores, indicating association with disease severity.
- In LPS-induced THP-1 cells, PSTPIP2 transfection decreased levels of IL-6, IL-1β, and TNF-α and inhibited NF-κB pathway activation.
Conclusions:
- PSTPIP2 expression is reduced in pressure ulcer sepsis and is associated with disease severity.
- PSTPIP2 demonstrates anti-inflammatory properties by modulating cytokine production and NF-κB signaling.
- PSTPIP2 may represent a potential therapeutic target for managing inflammation in pressure ulcer sepsis.
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