Τίτλος:
Immunomodulation Through Beta-D-glucan in Chemically-induced Necrotizing Pancreatitis
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Background: Although the ability of β-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 β-D-glucan 3 d before pancreatitis, C: pretreatment with MPLA 3 d before pancreatitis, D: pretreatment with β-D-glucan and laminarin 3 d before pancreatitis, E: treatment with β-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 β-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 β-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 β-D- glucan. Conclusions: β-D-glucan reduces mortality of experimental pancreatitis in vivo. This is mediated through attenuation of cytokine production and prevention of bacterial translocation. © 2020 Elsevier Inc.
Συγγραφείς:
Koliakos, N.N.
Renieris, G.
Sotiropoulos, D.
Pavlou, K.
Droggiti, D.-E.
Gkavogianni, T.
Charalampopoulos, A.
Giamarellos-Bourboulis, E.J.
Περιοδικό:
Journal of Surgical Research
Εκδότης:
Academic Press Inc.
Λέξεις-κλειδιά:
alvet; amylase; beta glucan; dectin 1; interleukin 10; ketamine; laminaran; lapretolimod; meloxicam; O antigen; paracetamol; taurocholic acid; toll like receptor 4; tumor necrosis factor; xylazine; amylase; glucan; immunological adjuvant; laminaran; lipid A; polysaccharide-K; proteoglycan; tumor necrosis factor, acclimatization; acute hemorrhagic pancreatitis; amylase blood level; animal experiment; animal model; Article; bacterium colony; controlled study; density gradient; disease exacerbation; experimental pancreatitis; immunomodulation; immunotherapy; Leporidae; male; nonhuman; pancreas tissue; pancreatic duct; parenchyma; peripheral blood mononuclear cell; polymorphonuclear cell; priority journal; acute hemorrhagic pancreatitis; animal; bacterial translocation; blood; drug effect; metabolism; mortality; preclinical study, Adjuvants, Immunologic; Amylases; Animals; Bacterial Translocation; Drug Evaluation, Preclinical; Glucans; Immunomodulation; Lipid A; Male; Pancreatitis, Acute Necrotizing; Proteoglycans; Rabbits; Taurocholic Acid; Tumor Necrosis Factor-alpha
DOI:
10.1016/j.jss.2020.12.020
