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Metaproteomic analysis of non-IBD, UC and pouchitis patients stool samples berfore and on antibiotics treatment

ABSTRACT: Antibiotics (Abx) are critical in modern medicine but can induce intestinal dysbiosis, exacerbate inflammatory bowel diseases (IBD), and disrupt the gut microbiome. Moreover, Abx treatment was reported as a significant risk factor for developing IBD, yet the underlying mechanisms remain unknown. Here, we employed metagenomics and metaproteomics to investigate the impact of Abx treatment on gut microbiota composition and activity in non-IBD, pouchitis, and ulcerative colitis (UC) patients. The combined analysis revealed distinct microbiome profiles for each group and found that the metaproteomes are more susceptible to Abx-induced changes than metagenomes. Alpha diversity decreased across all cohorts during Abx treatment, with pouchitis and UC patients exhibiting dysbiosis before treatment. Taxonomic shifts, including blooms of Proteobacteria and Actinobacteria, and reductions in microbial pathway abundances were more pronounced in IBD patients. Proteomic analysis revealed an elevated abundance of host pancreatic proteases, particularly in non-IBD patients, and during Antibiotic treatment, correlating with increased proteolytic activity and impaired gut barrier function. Functional assays confirm differential fecal proteolytic activity, suggesting that bacterial protease inhibitors, which are significantly depleted during Abx treatment, regulate proteolysis and thereby maintain delicate homeostasis in the gut. Overall, our findings suggest that Abx treatment disrupts the balance between bacterial protease inhibitors and host proteases, contributing to inflammation and gut barrier disruption. This work underscores the importance of understanding Abx-induced proteolytic shifts in the context of IBD and highlights the utility of metaproteomics in elucidating host-microbiome interactions. Future research should investigate the molecular mechanisms underlying the abundance and activity of bacterial protease inhibitors, as well as their impact on gut health.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Feces

SUBMITTER: Lior Lobel

LAB HEAD: Lior Lobel

PROVIDER: PXD066732 | Pride | 2026-04-29

REPOSITORIES: Pride

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Project description:Pancreatic cancer is the 3rd most prevalent cause of cancer related deaths in United states alone, with over 55000 patients being diagnosed in 2019 alone and nearly as many succumbing to it. Late detection, lack of effective therapy and poor understanding of pancreatic cancer systemically contributes to its poor survival statistics. Obesity and high caloric intake linked co-morbidities like type 2 diabetes (T2D) have been attributed as being risk factors for a number of cancers including pancreatic cancer. Studies on gut microbiome has shown that lifestyle factors as well as diet has a huge effect on the microbial flora of the gut. Further, modulation of gut microbiome has been seen to contribute to effects of intensive insulin therapy in mice on high fat diet. In another study, abnormal gut microbiota was reported to contribute to development of diabetes in Db/Db mice. Recent studies indicate that microbiome and microbial dysbiosis plays a role in not only the onset of disease but also in its outcome. In colorectal cancer, Fusobacterium has been reported to promote therapy resistance. Certain intra-tumoral bacteria have also been shown to elicit chemo-resistance by metabolizing anti-cancerous agents. In pancreatic cancer, studies on altered gut microbiome have been relatively recent. Microbial dysbiosis has been observed to be associated with pancreatic tumor progression. Modulation of microbiome has been shown to affect response to anti-PD1 therapy in this disease as well. However, most of the studies in pancreatic cancer and microbiome have remained focused om immune modulation. In the current study, we observed that in a T2D mouse model, the microbiome changed significantly as the hyperglycemia developed in these animals. Our results further showed that, tumors implanted in the T2D mice responded poorly to Gemcitabine/Paclitaxel (Gem/Pac) standard of care compared to those in the control group. A metabolomic reconstruction of the WGS of the gut microbiota further revealed that an enrichment of bacterial population involved in drug metabolism in the T2D group.

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Metaproteomic analysis of non-IBD, UC and pouchitis patients stool samples berfore and on antibiotics treatment

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