Pancreatitis

Fungal dysbiosis is a feature of acute pancreatitis, with altered intestinal fungal communities detected early in the disease course.

Bacterial translocation from a dysbiotic gut is a major driver of secondary pancreatic infection in severe AP.

16S rRNA sequencing of pancreatic infections identifies specific bacterial communities driving infectious complications.

Autoimmune pancreatitis (AIP) has a distinct fecal microbiota compared to pancreatic ductal adenocarcinoma (PDAC), despite overlapping clinical presentations. Shotgun metagenomics revealed differential functional profiles that may serve as diagnostic biomarkers.

mendelian randomization supports a causal relationship between specific gut microbiota and pancreatitis risk.

Meta-analysis of 13 RCTs found that probiotics, prebiotics, and synbiotics reduce infectious complications in severe acute pancreatitis. The mechanism likely involves:

Pancreatitis is inflammation of the pancreas, occurring as acute pancreatitis (AP, 34 per 100,000/year) and chronic pancreatitis (CP, 10 per 100,000). Severe AP carries 20-30% mortality, driven in large part by bacterial translocation from the dysbiotic gut to the pancreas. CP is the strongest non-genetic risk factor for pancreatic cancer (2.7-16x relative r

The pancreatitis signature is distinctive in two ways: (1) it involves both bacterial and fungal dysbiosis—candida albicans dominates the AP mycobiome, and (2) the gut-to-organ translocation pathway is central, with 16S rRNA sequencing identifying 660 bacterial strains in pancreatic infections from intestinal, oral, and airway origins.

Iron (elevated): Iron availability is relevant because the dominant pancreatic infection organisms (Klebsiella, E. coli, Pseudomonas) are highly siderophore-dependent. Parenteral nutrition in severe AP patients may provide unregulated iron that fuels pathobiont expansion. Candida species are also iron-dependent for morphogenesis and virulence.

Alcohol is the most common cause of AP, directly damaging pancreatic acinar cells and altering gut microbiome composition. MR analysis confirms bidirectional causation between gut microbiota and pancreatitis—pancreatitis itself causally increases Proteobacteria and Lachnospiraceae in the gut, while specific taxa causally increase pancreatitis risk. This bi

Gallstones (second most common cause) alter bile acid metabolism, which shapes gut microbial ecology. High-fat diets increase bile-resistant organisms including Bilophila and Alistipes.

Elevated WBC and IL-6: The systemic inflammatory response in AP is severe. Aspergillus abundance shows strong positive correlation with WBC counts, suggesting fungal-mediated immune activation.

Depleted butyrate: Fecal butyrate is significantly decreased in PDAC patients (confirmed by gas chromatography), and the Wood-Ljungdahl pathway (classical acetate production) is depleted.

Depleted SCFA synthesis capacity: The gut microbiome in pancreatitis/PDAC shows depleted metabolic capacity for SCFA synthesis at the functional level, not just at the taxonomic level.

Pancreatic infections in severe AP are polymicrobial in 98.21% of samples, with bacterial communities sourced from the intestines (43%), anaerobic reservoirs (43%), and oral cavity/airways (17%).

klebsiella pneumoniae is the dominant aerobic isolate (48.08% of samples), followed by acinetobacter baumannii, pseudomonas aeruginosa, and escherichia coli. All four are siderophore-producing Proteobacteria whose virulence depends on iron availability.

bacteroides fragilis is the dominant anaerobic isolate (16/56 patients), followed by B. kribbi, B. ovatus, and Dialister invisus.

MR-validated causal risk taxa include Coprococcus3 (OR=1.48), Eubacterium fissicatena group (OR=1.24), and Barnesiella (OR=1.48 for chronic pancreatitis).

candida albicans dominates the AP mycobiome (61.34%), followed by aspergillus (15.18%), Penicillium (5.98%), and Apiotrichum (5.23%). This is a dramatic shift from healthy controls where Aspergillus, Ganoderma, and Penicillium are dominant and Candida is minor.

faecalibacterium prausnitzii and roseburia intestinalis are depleted in PDAC. Eubacterium rectale is the top discriminating biomarker (AUC=90.74%) for distinguishing PDAC from healthy controls. The Firmicutes/Bacteroidetes ratio is decreased in PDAC.

MR-validated protective taxa include Prevotella9 (OR=0.82 for AP) and Ruminiclostridium6 (OR=0.70 for AP).

Type II secretion system: Enriched in PDAC gut microbiome functional analysis, enabling bacterial protein export and toxin delivery.

The central ecological event in severe AP is gut-to-pancreas bacterial translocation. A dysbiotic gut with compromised barrier integrity permits bacteria (and fungi) to reach the pancreas via portal circulation, lymphatics, and direct transmural migration. 16S rRNA sequencing reveals that pancreatic infections originate from the intestines (43%), anaerobic r

Pancreatic infection communities are not static—when sampling intervals exceed 2 weeks, bacterial composition changes significantly, and low-abundance species can become dominant pathogens. This temporal evolution has implications for antibiotic strategy.