Abstract
BACKGROUND: The objective of the current study was to elucidate the clinical mechanism through which phospholipase D2 (PLD2) exerted a regulatory effect on neutrophil migration, thereby alleviating the progression of acute pancreatitis. AIM: To elucidate the clinical mechanism through which PLD2 exerted a regulatory effect on neutrophil migration, thereby alleviating the progression of acute pancreatitis. METHODS: The study involved 90 patients diagnosed with acute pancreatitis, admitted to our hospital between March 2020 and November 2022. A retrospective analysis was conducted, categorizing patients based on Ranson score severity into mild (n = 25), moderate (n = 30), and severe (n = 35) groups. Relevant data was collected for each group. Western blot analysis assessed PLD2 protein expression in patient serum. Real-time reverse transcription polymerase chain reaction was used to evaluate the mRNA expression of chemokine receptors associated with neutrophil migration. Serum levels of inflammatory factors in patients were detected using enzyme-linked immunosorbent assay. Transwell migration tests were conducted to compare migration of neutrophils across groups and analyze the influence of PLD2 on neutrophil migration. RESULTS: Overall data analysis did not find significant differences between patient groups (P > 0.05). The expression of PLD2 protein in the severe group was lower than that in the moderate and mild groups (P < 0.05). The expression level of PLD2 in the moderate group was also lower than that in the mild group (P < 0.05). The severity of acute pancreatitis is negatively correlated with PLD2 expression (r = -0.75, P = 0.002). The mRNA levels of C-X-C chemokine receptor type 1, C-X-C chemokine receptor type 2, C-C chemokine receptor type 2, and C-C chemokine receptor type 5 in the severe group are significantly higher than those in the moderate and mild groups (P < 0.05), and the expression levels in the moderate group are also higher than those in the mild group (P < 0.05). The levels of C-reactive protein, tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the severe group were higher than those in the moderate and mild groups (P < 0.05), and the levels in the moderate group were also higher than those in the mild group (P < 0.05). The number of migrating neutrophils in the severe group was higher than that in the moderate and mild groups (P < 0.05), and the moderate group was also higher than the mild group (P < 0.05). In addition, the number of migrating neutrophils in the mild group combined with PLD2 inhibitor was higher than that in the mild group (P < 0.05), and the number of migrating neutrophils in the moderate group combined with PLD2 inhibitor was higher than that in the moderate group (P < 0.05). The number of migrating neutrophils in the severe group + PLD2 inhibitor group was significantly higher than that in the severe group (P < 0.05), indicating that PLD2 inhibitors significantly stimulated neutrophil migration. CONCLUSION: PLD2 exerted a crucial regulatory role in the pathological progression of acute pancreatitis. Its protein expression varied among patients based on the severity of the disease, and a negative correlation existed between PLD2 expression and disease severity. Additionally, PLD2 appeared to impede acute pancreatitis progression by limiting neutrophil migration.