Immunomodulation Through Beta-D-glucan in Chemically-induced Necrotizing Pancreatitis

Background: Although the ability of beta-D-glucan and monophosphoryl lipid A (MPLA) to modulate immune responses has been studied in human primary cells, their effect on sterile inflammation models such as necrotizing pancreatitis has never been investigated. Materials and methods: 85 male New Zealand rabbits were assigned into following groups: A: control, B: pretreatment with beta-D-glucan 3 d before pancreatitis, C: pretreatment with MPLA 3 d before pancreatitis, D: pretreatment with beta-D-glucan and laminarin 3 d before pancreatitis, E: treatment with beta-D-glucan 1 d after pancreatitis, and F: MPLA 1 d after pancreatitis. Pancreatitis was induced by sodium taurocholate injection into the pancreatic duct and parenchyma. Survival was recorded for 21 d. On days 1, 3, and 7, blood was collected for amylase measurement. Peripheral blood mononuclear cells were isolated and stimulated for tumor necrosis factor alpha and interleukin 10 production. Pancreatic necrosis and tissue bacterial load were assessed. Results: 21-d survival was prolonged after pretreatment or treatment with p-D-glucan; this benefit was lost with laminarin administration. At sacrifice, pancreatic inflammatory alterations were more prominent in the control group. Bacterial load was lower after pretreatment or treatment with beta-D-glucan and MPLA. Tumor necrosis factor alpha production from stimulated peripheral blood mononuclear cells was significantly decreased, whereas interleukin 10 production remained unaltered after pretreatment or treatment with beta-D-glucan. Conclusions: beta-D-glucan reduces mortality of experimental pancreatitis in vivo. This is mediated through attenuation of cytokine production and prevention of bacterial translocation. (C) 2020 Elsevier Inc. All rights reserved.

Automated summary

The study found that in experimental pancreatitis, pretreatment or treatment with beta-D-glucan can prolong survival and reduce bacterial load. After treatment, the production of tumor necrosis factor alpha was significantly decreased, while interleukin 10 production remained unchanged.