Article ; Online: Immunomodulation Through Beta-D-glucan in Chemically-induced Necrotizing Pancreatitis.
The Journal of surgical research
2021 Volume 261, Page(s) 74–84
Abstract: 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 ... ...
| Abstract | 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. |
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| MeSH term(s) | Adjuvants, Immunologic/pharmacology ; Adjuvants, Immunologic/therapeutic use ; Amylases/blood ; Animals ; Bacterial Translocation/drug effects ; Drug Evaluation, Preclinical ; Glucans ; Immunomodulation ; Lipid A/analogs & derivatives ; Lipid A/pharmacology ; Lipid A/therapeutic use ; Male ; Pancreatitis, Acute Necrotizing/blood ; Pancreatitis, Acute Necrotizing/drug therapy ; Pancreatitis, Acute Necrotizing/mortality ; Proteoglycans/pharmacology ; Proteoglycans/therapeutic use ; Rabbits ; Taurocholic Acid ; Tumor Necrosis Factor-alpha/metabolism |
| Chemical Substances | Adjuvants, Immunologic ; Glucans ; Lipid A ; Proteoglycans ; Tumor Necrosis Factor-alpha ; polysaccharide-K (3X48A86C8K) ; Taurocholic Acid (5E090O0G3Z) ; laminaran (9008-22-4) ; Amylases (EC 3.2.1.-) ; monophosphoryl lipid A (MWC0ET1L2P) |
| Language | English |
| Publishing date | 2021-01-07 |
| Publishing country | United States |
| Document type | Journal Article ; Research Support, Non-U.S. Gov't |
| ZDB-ID | 80170-7 |
| ISSN | 1095-8673 ; 0022-4804 |
| ISSN (online) | 1095-8673 |
| ISSN | 0022-4804 |
| DOI | 10.1016/j.jss.2020.12.020 |
| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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