Evaluation of acylated/deacylated ghrelin, CCL20/CCR6 concentration, and IgG N-Glycan alterations in different dysplasia grades of colon adenoma.

Colorectal adenomas represent precursor lesions in the adenoma-carcinoma sequence and are characterized by chronic low-grade inflammation. Chemokine CCL20/CCR6 signaling and metabolic hormone ghrelin have been implicated in colorectal tumorigenesis, while IgG glycosylation reflects systemic immune status. However, their interrelationship across different stages of adenoma dysplasia remains unclear. A total of 70 patients with histologically confirmed colorectal adenomas were stratified into low-grade (n = 36) and high-grade dysplasia (n = 34). Serum CCL20, CCR6, acylated and deacylated ghrelin concentrations were measured using enzyme immunoassay (ELISA), while IgG N-glycans were analyzed by hydrophilic interaction liquid chromatography-ultra performance liquid chromatography (HILIC-UPLC). Correlation analyses were performed to assess associations between inflammatory, metabolic, and glycomic parameters. No significant differences were observed between low- and high-grade dysplasia in circulating CCL20, CCR6, acylated or deacylated ghrelin, or IgG N-glycosylation profiles. A significant positive correlation between acylated and deacylated ghrelin was detected only in high-grade dysplasia. In low-grade dysplasia, CCL20 correlated significantly with deacylated ghrelin. Additional nominal associations between ghrelin, CCL20, and selected IgG glycan traits were identified but lost significance after Benjamini-Hochberg false discovery rate correction. These exploratory associations included bisecting glycans with deacylated ghrelin and CCL20 with GP20, GP21, GP1, and GP10. Although systemic inflammatory biomarkers, ghrelin isoforms, and IgG N-glycosylation did not differ between dysplasia grades, distinct correlation patterns suggest stage-specific relationships. The association between CCL20 and deacylated ghrelin in low-grade dysplasia and the strong correlation between ghrelin isoforms in high-grade dysplasia warrant further investigation.