Microbiome changes associated with acute and chronic pancreatitis: A systematic review

Brubaker, Lisa; Luu, Sommer; Kl, Hoffman; Wood, Amy Louise; Cagigas, Martha N.; Yao, Qizhi; Petrosino, Joe; Fisher, William E.; Buren, George Van

doi:10.1016/j.pan.2020.12.013

Cited by 17 publications

(14 citation statements)

References 45 publications

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“…Previous studies demonstrated that dysbiosis of intestinal microbiota was often associated with intestinal barrier dysfunction and metabolic disorders was observed during AP ( 87 ). Decreased beneficial bacteria and increased potentially pathogenic bacteria, such as E.coli and Enterococcus, may contribute to dysbiosis of intestinal microbiota and bacterial translocation ( 88 ). To confront the microenvironment dysbiosis, the intestine must develop a complex immune protection network including a variety of immune cells.…”

Section: Interaction Between Gut Microbiota and Immune Cells In Apmentioning

confidence: 99%

Role of Interleukin-17 in Acute Pancreatitis

Chen

Liu

et al. 2021

Front. Immunol.

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Acute pancreatitis (AP) is a leading cause of death and is commonly accompanied by systemic manifestations that are generally associated with a poor prognosis. Many cytokines contribute to pancreatic tissue damage and cause systemic injury. Interleukin-17 (IL-17) is a cytokine that may play a vital role in AP. Specifically, IL-17 has important effects on the immune response and causes interactions between different inflammatory mediators in the AP-related microenvironment. In this literature review, we will discuss the existing academic understanding of IL-17 and the impacts of IL-17 in different cells (especially in acinar cells and immune system cells) in AP pathogenesis. The clinical significance and potential mechanisms of IL-17 on AP deterioration are emphasized. The evidence suggests that inhibiting the IL-17 cytokine family could alleviate the pathogenic process of AP, and we highlight therapeutic strategies that directly or indirectly target IL-17 cytokines in acute pancreatitis.

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Section: Interaction Between Gut Microbiota and Immune Cells In Apmentioning

confidence: 99%

Role of Interleukin-17 in Acute Pancreatitis

Chen

Liu

et al. 2021

Front. Immunol.

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“…Patients with CP have altered gut microbiota where the diversity of the microbiome is found to be decreased. [ 31 , 32 ] Abdominal pain is the leading complication in CP patient population and is often worsened by food intake. This can over time lead to malnutrition, and CP patients frequently experience malabsorption and maldigestion.…”

Section: Discussionmentioning

confidence: 99%

Regional gastrointestinal transit times in patients with chronic pancreatitis

et al. 2022

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The mechanisms behind disrupted gastrointestinal (GI) motor function in patients with chronic pancreatitis (CP) have not been fully elucidated. We compared regional transit times in patients with CP to those in healthy controls, and investigated whether they were associated with diabetes mellitus, exocrine dysfunction, opioid treatment or quality of life. Twenty-eight patients with CP and 28 age- and gender-matched healthy controls were included. Regional GI transit times were determined using the 3D-Transit system, which consists of an ingestible electromagnetic capsule and a detector worn in an abdominal belt for 5 days. Exocrine function was assessed using the fecal elastase-1 test, and quality of life was assessed using the European Organization for Research and Treatment of Cancer questionnaire. Transit times were analyzed for associations with diabetes mellitus, exocrine pancreatic insufficiency (EPI), opioid treatment and quality of life. Compared with healthy controls, patients with CP had prolonged transit times in the small intestine (6.6 ± 1.8 vs 4.8 ± 2.2 hours, P = .006), colon (40 ± 23 vs 28 ± 26 hours, P = .02), and total GI tract (52 ± 26 vs 36 ± 26 hours, P = .02). There was no difference in gastric emptying time (4.8 ± 5.2 vs 3.1 ± 1.3 hours, P = .9). No associations between transit times and diabetes, EPI, or opioid consumption were found (all P > .05). Quality of life and associated functional and symptom subscales were not associated with transit times, except for diarrhea ( P = .03). Patients with CP have prolonged small intestinal and colonic transit times. However, these alterations do not seem to be mediated by diabetes, EPI, or opioid consumption.

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“…Типичными изменениями микробиоты толстой кишки при хроническом панкреатите являются уменьшение микробного разнообразия, увеличение доли Proteobacteria, снижение Bacteroidetes и бутират-продуцирующих бактерий (БПБ), таких как Faecalibacterium, значимая связь с инфекционными путями (по данным анализа с использованием Киотской энциклопедии генов и геномов [KEGG]), сопутствующими метаболическими заболеваниями (сахарный диабет) и экзокринной недостаточностью поджелудочной железы [10] (рис. 1).…”

Section: дисбиоз толстой кишки у взрослых пациентов с хроническим пан...unclassified

“…Дисбиотические изменения микробиоты толстой кишки при хроническом панкреатите; триггеры/факторы риска развития хронического панкреатита: длительное употребление алкоголя, курение, метаболические и сосудистые расстройства, аутоиммунные заболевания, генетические нарушения [6,8,9,10] (в модификации).…”

Section: рисунокunclassified

“…Рост условно-патогенных бактерий Потеря продуцентов бутирата и других КЖК с тяжестью заболевания. По мнению некоторых исследователей, отсутствие явной связи между этиологией хронического панкреатита и изменениями микробиома при положительной корреляции между тяжестью заболевания и этими изменениями позволяет предположить, что дисбиоз толстой кишки является скорее результатом хронического панкреатита, а не его причиной[8,10]. Следует отметить, что дисбиоз толстой кишки, в свою очередь, может привести к развитию СИБР[8].…”

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Chronic pancreatitis and the intestinal microbiome in adults and children: Not only SIBO but also gut dysbiosis has clinical significance

Sitkin

Pervunina

2022

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Chronic pancreatitis is accompanied by both small intestinal bacterial overgrowth and dysbiosis of the gut microbiota. The most typical changes in the gut microbiota in chronic pancreatitis are a decrease in microbial diversity, an increase in the abundance of Proteobacteria, a decrease in the abundance of Bacteroidetes, Actinobacteria, and Firmicutes, especially butyrate-producing bacteria such as Faecalibacterium, a significant association with infectious pathways (KEGG analysis]), concomitant metabolic disorders (diabetes mellitus) and exocrine pancreatic insufficiency. Changes in the gut microbiota in children with chronic pancreatitis are like those in adults and are characterized by a decrease in α-diversity and the loss of shortchain fatty acid producers: butyrate-producing Faecalibacterium, Subdoligranulum, and Eubacterium, propionate-producing Phascolarctobacterium, acetate- and lactate-producing Collinsella, and probiotic Bifidobacterium. Dysbiotic changes in the gut microbiome, including a decrease in the abundance of commensal symbionts, are significantly associated with the severity of chronic pancreatitis. The most important factor influencing the intestinal microbiota is the pancreatic exocrine function, a decrease which leads to a switch from enterotype 1 (Bacteroides predominance) to enterotype 2 (Prevotella predominance) and a decrease in phylogenetic diversity (α-diversity index). Modulation of the dysbiotic gut microbiota can be carried out with probiotics, prebiotics, bacterial metabolites such as butyrate, pancreatic enzymes and should become a full-fledged therapeutic option in patients with chronic pancreatitis.

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Microbiome changes associated with acute and chronic pancreatitis: A systematic review

Cited by 17 publications

References 45 publications

Role of Interleukin-17 in Acute Pancreatitis

Role of Interleukin-17 in Acute Pancreatitis

Regional gastrointestinal transit times in patients with chronic pancreatitis

Chronic pancreatitis and the intestinal microbiome in adults and children: Not only SIBO but also gut dysbiosis has clinical significance

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