Abstract
Background Chronic diabetic foot ulcer (DFU) is one of the most intractable complications of diabetes mellitus (DM). Its pathogenesis is complex, and uncontrolled chronic inflammation is an important factor. Endothelial overexpressed lipopolysaccharide-associated factor 1 (EOLA1) discovered in our laboratory is an intracellular protein with the function of inflammatory regulation. This study was aimed at observing the expression of EOLA1 in DFU skin tissues and its relationship with inflammation and at exploring the possible role of EOLA1 in DFU and its mechanism. Methods The patients with DFU were divided into 2 groups based on the formation time of ulcer: the acute wound (AW) group with the course of disease ≤ 4 weeks and the chronic wound (CW) group with the course of disease > 4 weeks. The relevant clinical data of patients were collected, and the skin tissues around the ulcer were used for immunofluorescence detection and immunohistochemical staining to observe inflammation. The expression levels of EOLA1, metallothionein 2A (MT2A), nuclear factor-κB (NF-κB), and interleukin-6 (IL-6) were detected by western blot. Results A total of 79 patients were enrolled in the study. The results of immunofluorescence and immunohistochemistry showed that EOLA1 was expressed in the epithelial tissues of DFU. However, the expression of EOLA1 in the CW group was significantly lower than that in the AW group (P < 0.05), and the expression of NF-κB and IL-6 was obviously increased (P < 0.05). Conclusion The refractory wounds in patients with DFU may be closely related to the uncontrolled activation of inflammatory pathways in cells caused by the reduced expression of negative regulators of inflammation (e.g., EOLA1), and such decreased expression may be also strongly linked to the persistent state of inflammation.
Highlights
With the high rates of disability and death, chronic diabetic foot ulcer (DFU) is one of the most refractory complications of diabetes mellitus (DM), and it seriously affects the patients’ quality of life and life expectancy [1]
The main cause for DFU is a protracted course of inflammation in wounds, which is manifested as reduced apoptosis of inflammatory cells, abnormal phenotypic transformation of macrophage M1/M2, and failure to timely terminate the inflammatory signaling pathway of intracellular activated nuclear factor-κB (NF-κB)
No statistically significant difference was observed in the plasma inflammatory indicators, high-sensitivity C-reactive protein (HsCRP) (t = 0 25, P = 0 80), PCT (t = 1 48, P = 0 16), IL-6 (t = 0 04, P = 0 97), white blood cells (WBC) (t = −0 54, P = 0 09), and NE% (t = 0 41, P = 0 68)
Summary
With the high rates of disability and death, chronic diabetic foot ulcer (DFU) is one of the most refractory complications of diabetes mellitus (DM), and it seriously affects the patients’ quality of life and life expectancy [1]. The main cause for DFU is a protracted course of inflammation in wounds, which is manifested as reduced apoptosis of inflammatory cells, abnormal phenotypic transformation of macrophage M1/M2, and failure to timely terminate the inflammatory signaling pathway of intracellular activated nuclear factor-κB (NF-κB). The relevant clinical data of patients were collected, and the skin tissues around the ulcer were used for immunofluorescence detection and immunohistochemical staining to observe inflammation. The results of immunofluorescence and immunohistochemistry showed that EOLA1 was expressed in the epithelial tissues of DFU. The refractory wounds in patients with DFU may be closely related to the uncontrolled activation of inflammatory pathways in cells caused by the reduced expression of negative regulators of inflammation (e.g., EOLA1), and such decreased expression may be strongly linked to the persistent state of inflammation
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