ArticleGut microbes
Paclitaxel chemotherapy disrupts microbiota-enterohepatic bile acid metabolism in mice.
Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- A systematic assessment of the short- and long-term effects of commonly used breast cancer chemotherapeutics on the gut microbiome‒blood‒brain axis of female mice.Gut microbes · 2026Article
- Tamoxifen induced hepatotoxicity via gut microbiota-mediated hyodeoxycholic acid depletion and Farnesoid X receptor signaling disruption.Gut microbes · 2026Article
- Gut microbiota and metabolite disruption during breast cancer chemotherapy is associated with peripheral neuropathy sensory symptoms and pain.Brain, behavior, and immunity · 2026Article
- Gut-to-bile transfer of microbially amidated minor bile acids in patients with hepatopancreatobiliary disorders.Hepatology (Baltimore, Md.) · 2026Article
- Dysregulation of the AMPK-SREBP1-FASN axis in MASLD: driving a vicious cycle of lipotoxicity and metabolic-immune crosstalk.Lipids in health and disease · 2026Review
- A Glutathione-Responsive Prodrug Nanosystem for Colorectal Cancer: Synergistic Co-Delivery of Paclitaxel and Curcumin to Combat Multidrug Resistance and Reinvent the Immunosuppressive Microenvironment.Biomaterials research · 2026Article
- CircERC1 facilitates chemoresistance through inhibiting pyroptosis and remodeling extracellular matrix in pancreatic cancer.Molecular cancer · 2025Article
- Strain-dependent neuronal disposition and toxicity of paclitaxel in mice.ASPET discovery · 2025Article
- Bile's Hidden Weapon: Modulating the Microbiome and Tumor Microenvironment.Current microbiology · 2024Review
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Authors and funding
9 authors.
Funding
Abstract
Balanced interactions between the enteric microbiota and enterohepatic organs are essential to bile acid homeostasis, and thus normal gastrointestinal function. Disruption of these interactions by cancer treatment instigates bile acid malabsorption, leading to treatment delays, malnutrition, and decreased quality of life. However, the nature of chemotherapy-induced bile acid malabsorption remains poorly characterized with limited treatment options. Therefore, this study sought to characterize changes in hepatic, enteric, and microbial bile acid metabolism in a mouse model of chemotherapy-induced toxicity. Consistent with clinical bile acid malabsorption, chemotherapy increased fecal excretion of primary bile acids and water, while diminishing microbiome diversity, secondary bile acid formation, and small intestinal bile acid signaling. We identified new contributors to pathology of bile acid malabsorption in the forms of lipopolysaccharide-induced cholestasis and colonic crypt hyperplasia from reduced secondary bile acid signaling. Chemotherapy reduced markers of hepatic bile flow and bile acid synthesis, elevated markers of fibrosis and endotoxemia, and altered transcription of genes at all stages of bile acid metabolism. Primary hepatocytes exposed to lipopolysaccharide (but not chemotherapy) replicated chemotherapy-induced transcriptional differences, while gut microbial transplant into germ-free mice replicated very few differences. In the colon, chemotherapy-altered bile acid profiles (particularly higher tauromuricholic acid and lower hyodeoxycholic acid) coincided with crypt hyperplasia. Exposing primary colonoids to hyodeoxycholic acid reduced proliferation, while gut microbiota transplant enhanced proliferation. Together, these investigations reveal complex involvement of the entire microbiota-enterohepatic axis in chemotherapy-induced bile acid malabsorption. Interventions to reduce hepatic lipopolysaccharide exposure and enhance microbial bile acid metabolism represent promising co-therapies to cancer treatment.
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