Hypertriglyceridemia-associated acute pancreatitis (HTGAP) is linked with increased severity and morbidity. Intestinal flora plays an important role in the progression of acute pancreatitis (AP). However, pathogenetic association between gut microbiota and HTGAP remains unknown. In this study, we enrolled 30 HTGAP patients and 30 patients with AP that is evoked by other causes. The V3–V4 regions of 16S rRNA sequences of the gut microbiota were analyzed. Clinical characteristics, microbial diversity, taxonomic profile, microbiome composition, microbiological phenotype, and functional pathways were compared between the two groups. Our results showed that the HTGAP group had a higher proportion of severe AP (46.7% vs. 20.0%), organ failure (56.7% vs. 30.0%), and a longer hospital stay (18.0 days vs. 6.5 days). HTGAP group also had poorer microbial diversity, higher abundances of Escherichia/Shigella and Enterococcus, but lower abundances of Dorea longicatena, Blautia wexlerae, and Bacteroides ovatus as compared with non-HTGAP group. Correlation analysis revealed that gut bacterial taxonomic and functional changes were linked with local and systemic complications, ICU admission, and mortality. This study revealed that alterations of gut microbiota were associated with disease severity and poor prognosis in HTGAP patients, indicating a potential pathophysiological link between gut microbiota and hypertriglyceridemia related acute pancreatitis.

While emerging evidence highlights the significance of gut microbiome in gastrointestinal infectious diseases, treatments like Fecal Microbiota Transplantation (FMT) and probiotics are gaining popularity, especially for diarrhea patients. However, the specific role of the gut microbiome in different gastrointestinal infectious diseases remains uncertain. There is no consensus on whether gut modulation therapy is universally effective for all such infections. In this comprehensive review, we examine recent developments of the gut microbiome’s involvement in several gastrointestinal infectious diseases, including infection of Helicobacter pylori, Clostridium difficile, Vibrio cholerae, enteric viruses, Salmonella enterica serovar Typhimurium, Pseudomonas aeruginosa Staphylococcus aureus, Candida albicans, and Giardia duodenalis. We have also incorporated information about fungi and engineered bacteria in gastrointestinal infectious diseases, aiming for a more comprehensive overview of the role of the gut microbiome. This review will provide insights into the pathogenic mechanisms of the gut microbiome while exploring the microbiome’s potential in the prevention, diagnosis, prediction, and treatment of gastrointestinal infections.

Pancreatic repair after acute pancreatitis (AP) is essential for restoring tissue integrity, but the intrinsic mechanisms coordinating acinar plasticity and regeneration remain poorly understood. Aberrant Ca ^{2 +} signaling drives acinar injury, but whether Ca ^{2 +} ‐responsive effectors regulate post‐injury repair remains unclear. This study identifies calcium/calmodulin‐dependent protein kinase II δ (CaMKIIδ) as a repair‐associated regulator of pancreatic regeneration. Global Camk2d deletion delays repair after caerulein‐induced AP without altering initial injury severity. Bone marrow chimeras and pancreas‐specific Camk2d deletion further demonstrate that pancreatic, rather than bone marrow‐derived, CaMKIIδ is required for efficient tissue repair. Transcriptomic and ultrastructural analyses reveal that Camk2d deficiency disrupts endoplasmic reticulum (ER) homeostasis and enhances PERK‐dependent unfolded protein response activation. Camk2d ‐deficient pancreas shows impaired acinar‐to‐ductal metaplasia (ADM) programs in vivo and defective ADM formation in ex vivo 3D culture. Integrated proteomic and phosphoproteomic profiling of acinar‐derived ADM identifies ancient ubiquitous protein 1 (AUP1), an ER‐associated degradation regulator, as a previously unrecognized CaMKIIδ‐dependent substrate candidate. Functional analyses show that phosphorylation of the AUP1 S280‐containing serine‐rich region promotes K48‐linked ubiquitination and restrains PERK‐dependent ER stress under pancreatic stress conditions. These findings define a CaMKIIδ–AUP1 axis linking Ca ^{2 +} ‐responsive kinase activity to ER proteostasis, ADM formation and pancreatic repair.