Gut microbiota aggravates neutrophil extracellular traps-induced pancreatic injury in hypertriglyceridemic pancreatitis

Li, Guanqun; Liu, Liwei; Lu, Tianqi; Sui, Yuhang; Zhang, Can; Wang, Yongwei; Zhang, Tao; Xie, Yu; Xiao, Peng; Zhao, Zhongjie; Cheng, Chundong; Hu, Jisheng; Chen, Hongze; Xue, Dongbo; Chen, Hua; Wang, Gang; Kong, Rui; Tan, Hongtao; Bai, Xuewei; Li, Zhibo; McAllister, Florencia; Li, Le; Sun, Bei

doi:10.1038/s41467-023-41950-y

Cited by 9 publications

(4 citation statements)

References 65 publications

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“…The abundances of Enterococcaceae and Escherichia Shigella were higher, while the abundances of Bacteroides and Faecalibacterium were lower. Correlation analysis showed that the abundances of Faecalibacterium and Bacteroides uniformis were negatively associated with disease severity [21]. These suggest that different type-dependent bacteria species affect AP development, and the unique gut microbial identity may determine the different outcomes.…”

Section: The Altered Microbial Community and Different Etiologiesmentioning

confidence: 85%

The Interaction of Microbiome and Pancreas in Acute Pancreatitis

Zhang,

Li,

et al. 2023

Biomolecules

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Acute pancreatitis (AP) is a common acute abdomen disease characterized by the pathological activation of digestive enzymes and the self-digestion of pancreatic acinar cells. Secondary infection and sepsis are independent prognosticators for AP progression and increased mortality. Accumulating anatomical and epidemiological evidence suggests that the dysbiosis of gut microbiota affects the etiology and severity of AP through intestinal barrier disruption, local or systemic inflammatory response, bacterial translocation, and the regulatory role of microbial metabolites in AP patients and animal models. Recent studies discussing the interactions between gut microbiota and the pancreas have opened new scopes for AP, and new therapeutic interventions that target the bacteria community have received substantial attention. This review concentrates on the alterations of gut microbiota and its roles in modulating gut–pancreas axis in AP. The potential therapies of targeting microbes as well as the major challenges of applying those interventions are explored. We expect to understand the roles of microbes in AP diagnosis and treatment.

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Section: The Altered Microbial Community and Different Etiologiesmentioning

confidence: 85%

The Interaction of Microbiome and Pancreas in Acute Pancreatitis

Zhang,

Li,

et al. 2023

Biomolecules

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“…These microbiota changes were related to the poor prognosis of HTGAP [ 43 ], which may suggest that the alterations in gut microbiota patterns are influenced not only by the pancreatitis itself, but also by its causative factor [ 43 , 44 ]. Although the specific mechanisms by which hypertriglyceridemia exacerbates the progression of AP remain unclear, excessive production of free fatty acids is hypothesized to lead to oxidative stress, vascular endothelial injury, pancreatic necrosis, and systemic inflammatory response [ 43 , 46 , 47 ].…”

Section: Gut Microbiota Profile In Pancreatitismentioning

confidence: 99%

Exploring the Microbial Landscape: Gut Dysbiosis and Therapeutic Strategies in Pancreatitis—A Narrative Review

Lupu,

Bratu,

Trandafir

et al. 2024

Biomedicines

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The gut microbiota is emerging as an important contributor to the homeostasis of the human body through its involvement in nutrition and metabolism, protection against pathogens, and the development and modulation of the immune system. It has therefore become an important research topic in recent decades. Although the association between intestinal dysbiosis and numerous digestive pathologies has been thoroughly researched, its involvement in pancreatic diseases constitutes a novelty in the specialized literature. In recent years, growing evidence has pointed to the critical involvement of the pancreas in regulating the intestinal microbiota, as well as the impact of the intestinal microbiota on pancreatic physiology, which implies the existence of a bidirectional connection known as the “gut–pancreas axis”. It is theorized that any change at either of these levels triggers a response in the other component, hence leading to the evolution of pancreatitis. However, there are not enough data to determine whether gut dysbiosis is an underlying cause or a result of pancreatitis; therefore, more research is needed in this area. The purpose of this narrative review is to highlight the role of gut dysbiosis in the pathogenesis of acute and chronic pancreatitis, its evolution, and the prospect of employing the microbiota as a therapeutic intervention for pancreatitis.

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“…Emerging research suggests a correlation between gut microbiota dysbiosis and conditions such as hepatitis, coronary heart disease, diabetes, and pancreatitis [10][11][12][13]. Li et al demonstrated in a mouse model of hypertriglyceridemic pancreatitis (HTGP) that gut microbiota colonization resulted in the recruitment of neutrophils and enhanced formation of neutrophil extracellular traps (NETs), ultimately exacerbating pancreatic injury and systemic in ammation [14]. Furthermore, Wang et al discovered that lactulose alters the gut microbiota composition and stimulates the production of short-chain fatty acids, consequently mitigating the advancement of pancreatitis [15].…”

Section: Introductionmentioning

confidence: 99%

A bidirectional two-sample Mendelian randomization using the gut microbiota to reveal potential therapeutic targets for acute pancreatitis

He,

Luo,

et al. 2024

Preprint

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Background: Numerous studies have indicated a correlation between the gut microbiota (GM) and acute pancreatitis (AP), yet the precise causal relationship between them remains ambiguous. Methods: A two-sample Mendelian randomization (MR) study was conducted utilizing aggregated data from genome-wide association studies (GWASs) of 471 taxa (11 phyla, 19 orders, 24 orders, 62 families, 146 genera, and 209 species) and AP patients. Various methods, including inverse variance weighting (IVW), MR‒Egger, weighted medians, simple mode, and weighted mode, were employed to assess the causal association between the GM and AP. Sensitivity analyses were conducted utilizing Cochran's Q test, MR-Egger regression intercept analysis, and MR-PRESSO, followed by reverse MR analysis to evaluate the potential reverse causality between AP and GM. Results: Three gut microbial taxa were found to have significant associations with acute pancreatitis (AP). The inverse variance weighted (IVW) results revealed that Coprobacillus (OR 1.19, 95% CI 1.01 to 1.40, p=0.035) and Holdemania sp900120005 (OR 1.18, 95% CI 1.02 to 1.35, p=0.023) were identified as risk factors for the development of AP, while Megamonas (OR: 0.87, 95% CI: 0.77 to 0.98, p=0.023) was found to be a protective factor against the occurrence of AP. A thorough sensitivity analysis confirmed the reliability of our findings. Reverse Mendelian randomization (MR) analysis did not indicate any causal relationship between AP and the gut microbiota (GM). Conclusions: This study revealed a complex causal relationship between 3 GM taxa and AP, providing new evidence for the development of AP from a genetic perspective.

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Gut microbiota aggravates neutrophil extracellular traps-induced pancreatic injury in hypertriglyceridemic pancreatitis

Cited by 9 publications

References 65 publications

The Interaction of Microbiome and Pancreas in Acute Pancreatitis

The Interaction of Microbiome and Pancreas in Acute Pancreatitis

Exploring the Microbial Landscape: Gut Dysbiosis and Therapeutic Strategies in Pancreatitis—A Narrative Review

A bidirectional two-sample Mendelian randomization using the gut microbiota to reveal potential therapeutic targets for acute pancreatitis

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