The Interaction of Microbiome and Pancreas in Acute Pancreatitis

Zhang, Can; Li, Guanqun; Lu, Tianqi; Liu, Liwei; Sui, Yuhang; Bai, Rui; Li, Le; Sun, Bei

doi:10.3390/biom14010059

Cited by 12 publications

(4 citation statements)

References 110 publications

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“…Through intestinal barrier disruption, local or systemic inflammation, bacterial translocation, and the regulation of microbial metabolites, dysbiosis of gut microbiota influences the etiology 15 . As compared to healthy volunteers, acute pancreatitis patients had more Bacteroidetes and Proteobacteria and fewer Firmicutes and Actinobacteria 37 .…”

Section: Discussionmentioning

confidence: 99%

“…Microbiota dysbiosis contributes to the etiology and severity of AP through intestinal barrier disruption, local or systemic inflammatory responses, and bacterial translocation. The interaction between gut microbiota and the pancreas has opened new avenues for AP, and new therapeutic interventions that target the bacteria community have been studied extensively 15 . Early dysbiosis in the gut microbiota may exacerbate the severity of AP.…”

Section: Introductionmentioning

confidence: 99%

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A purified membrane protein Amuc_1098 from Akkermansia muciniphila blunts acute pancreatitis by modulation of intestinal flora and glycerophospholipid metabolism

Wang,

Zhang,

Zhao

et al. 2024

Preprint

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Amuc_1098 is a membrane protein from Akkermansia muciniphila. In this study, we investigated how Amuc_1098 affects acute pancreatitis (AP) in mice induced by caerulein and lipopolysaccharide (LPS). Treating mice with Amuc_1098 (3 μg, i.g.) for 20 days before caerulein and LPS injection reduced pancreatic injury and lowered serum amylase and lipase levels. Amuc_1098 supplementation reduced proinflammatory cytokines (TNF-α, IL-1β and IL-6) in spleen and pancreas by inhibiting NF-κB signaling. It also decreased Ly6C+ macrophages in the spleen and pancreas of AP mice. Amuc_1098 pretreatment reversed declined tight junction proteins in the colon of AP mice. Glycerophospholipid metabolism was significantly increased in patients and mice with AP. We further demonstrated that oral administration of Amuc_1098 reduced glycerophospholipid metabolism enrichment mediated by intestinal flora. These results provide new evidence that Amuc_1098 lessens the severity of AP through its anti-inflammatory properties with a reduction of macrophage infiltration in spleen and pancreas, an elevation of tight junction proteins in the colon, as well as its regulation of the composition of intestinal flora and glycerophospholipid metabolism.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

A purified membrane protein Amuc_1098 from Akkermansia muciniphila blunts acute pancreatitis by modulation of intestinal flora and glycerophospholipid metabolism

Wang,

Zhang,

Zhao

et al. 2024

Preprint

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“…AP leads to an imbalance in the intestinal microbiota, exacerbating pancreatic harm and systemic inflammatory reactions. In this context, FMT offers a promising approach to diminish tissue damage and inflammation and to mitigate the dysbiosis [50,90].…”

Section: Acute and Chronic Pancreatitismentioning

confidence: 99%

The Importance of Microbiota and Fecal Microbiota Transplantation in Pancreatic Disorders

Boicean,

Ichim,

Todor

et al. 2024

Diagnostics

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The role of the intestinal microbiota in the diagnosis and treatment of pancreatic diseases is increasingly significant. Consequently, fecal microbiota transplantation (FMT) is emerging as a promising therapeutic avenue for various pancreatic disorders, including cancer, pancreatitis, and type 1 diabetes (T1D). This innovative procedure entails transferring gut microbiota from healthy donors to individuals affected by pancreatic ailments with the potential to restore intestinal balance and alleviate associated symptoms. FMT represents a pioneering approach to improve patient outcomes in pancreatic diseases, offering tailored treatments customized to individual microbiomes and specific conditions. Recent research highlights the therapeutic benefits of targeting the gut microbiota for personalized interventions in pancreatic disorders. However, a comprehensive understanding of the intricate interplay between gut microbiota and pancreatic physiology warrants further investigation. The necessity for additional studies and research endeavors remains crucial, especially in elucidating both adult and pediatric cases affected by pathological pancreatic conditions.

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“…Acute pancreatitis (AP) represents an acute inflammatory disorder of the pancreatic tissue that may not only affect nearby regional tissues but also extend its impact to remote organ systems, potentially resulting in systemic inflammation [ 1 , 2 ]. AP stands as a prevalent gastrointestinal reason for hospital admissions, with an annual incidence ranging from 20 to 40 cases per 100,000 individuals [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Redefining Immune Dynamics in Acute Pancreatitis: The Protective Role of Galectin-3 Deletion and Treg Cell Enhancement

Milivojcevic Bevc,

Tasic-Uros,

Stojanovic

et al. 2024

Biomolecules

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Acute pancreatitis (AP) is a complex inflammatory condition that can lead to systemic inflammatory responses and multiple organ dysfunction. This study investigates the role of Galectin-3 (Gal-3), a β-galactoside-binding lectin, in modulating acquired immune responses in AP. Acute pancreatitis was induced by ligation of the bile-pancreatic duct in wild-type and Galectin-3-deficient C57BL/6 mice. We determined the phenotypic and molecular features of inflammatory cells, serum concentrations of amylase, pancreatic trypsin activity, and pancreatic and lung pathology. Galectin-3 deficiency decreased the total number of CD3+CD49− T cells and CD4+ T helper cells, downregulated the production of inflammatory cytokine and IFN-γ, and increased the accumulation of IL-10-producing Foxp3+ T regulatory cells and regulatory CD4+ T cells in the pancreata of diseased animals. The deletion of Galectin-3 ameliorates acute pancreatitis characterized by lowering serum amylase concentration and pancreatic trypsin activity, and attenuating of the histopathology of the lung. These findings shed light on the role of Galectin-3 in acquired immune response in acute pancreatitis and identify Galectin-3 as an attractive target for investigation of the immunopathogenesis of disease and for consideration as a potential therapeutic target for patients with acute inflammatory disease of the pancreas.

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The Interaction of Microbiome and Pancreas in Acute Pancreatitis

Cited by 12 publications

References 110 publications

A purified membrane protein Amuc_1098 from Akkermansia muciniphila blunts acute pancreatitis by modulation of intestinal flora and glycerophospholipid metabolism

A purified membrane protein Amuc_1098 from Akkermansia muciniphila blunts acute pancreatitis by modulation of intestinal flora and glycerophospholipid metabolism

The Importance of Microbiota and Fecal Microbiota Transplantation in Pancreatic Disorders

Redefining Immune Dynamics in Acute Pancreatitis: The Protective Role of Galectin-3 Deletion and Treg Cell Enhancement

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