Background and aim: Low-grade inflammation persists in patients with acute pancreatitis (AP) after hospital discharge, and is linked to metabolic disorders. Neuropeptide Y (NPY) is well recognized as an important mediator of inflammation in these patients but the role of the other two structurally similar peptides, pancreatic polypeptide (PP) and peptide YY (PYY), in inflammation has been sparsely investigated. The aim was to investigate the association between PYY, PP, NPY and circulating levels of innate cytokines in patients after AP.Methods: Fasting blood samples were collected to measure PYY (ng/mL), PP (ng/mL), NPY (pg/mL), interleukin-6 (IL-6) (ng/mL), monocyte chemoattractant protein (MCP) 1 (ng/mL), and tumour necrosis factor (TNF) a (ng/mL). Modified Poisson regression analysis and linear regression analyses were conducted. Age, sex, ethnicity, obesity, diabetes, aetiology, time from 1st attack of AP, recurrence, severity, physical activity, and smoking were adjusted for in several statistical models. P < 0.05 was considered statistically significant.Results: A total of 93 patients were recruited. Peptide YY was significantly associated (p < 0.001) with IL 6, MCP-1, and TNF alpha in the unadjusted and all adjusted models. Pancreatic polypeptide was significantly associated (p < 0.001) with IL-6, MCP-1, and TNFa in the unadjusted and at least one adjusted model. Peptide YY and PP together contributed 22.2%, 72.7%, and 34.6% to the variance of IL-6, MCP-1, and TNF alpha, respectively. Neuropeptide Y was not significantly associated with any of the three cytokines.Conclusions: Peptide YY and PP are associated with circulating innate pro-inflammatory cytokines in patients after AP and cumulatively contribute to nearly half of the variance of IL-6, MCP-1, and TNF alpha. Future research is warranted to investigate the signaling pathways that underlie these associations. (C) 2016 Elsevier Ltd. All rights reserved.