ArticlePloS one2017
Depletion of enteric bacteria diminishes leukocyte infiltration following doxorubicin-induced small intestinal damage in mice.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Changes in gut, microbiome, and cognition after doxorubicin, cyclophosphamide, and paclitaxel chemotherapy treatment.Scientific reports · 2026Article
- Chemotherapy-Induced Neuropathy Affecting the Gastrointestinal Tract.Neurogastroenterology and motility · 2025Review
- Article
- Mechanisms driving fasting-induced protection from genotoxic injury in the small intestine.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Myeloperoxidase is a critical mediator of anthracycline-induced cardiomyopathy.Basic research in cardiology · 2023Article
- Varied effects of doxorubicin (DOX) on the corpus luteum of C57BL/6 mice during early pregnancy†.Biology of reproduction · 2021Article
- Attenuation of Doxorubicin-Induced Small Intestinal Mucositis by Pectins is Dependent on Pectin's Methyl-Ester Number and Distribution.Molecular nutrition & food research · 2021Article
- Doxorubicin increases permeability of murine small intestinal epithelium and cultured T84 monolayers.Scientific reports · 2020Article
- Polychemotherapy with Curcumin and Doxorubicin via Biological Nanoplatforms: Enhancing Antitumor Activity.Pharmaceutics · 2020Review
- Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsWhile enteric bacteria have been shown to play a critical role in other forms of intestinal damage, their role in mediating the response to the chemotherapeutic drug Doxorubicin (Doxo) is unclear. In this study, we used a mouse model of intestinal bacterial depletion to evaluate the role enteric bacteria play in mediating Doxo-induced small intestinal damage and, more specifically, in mediating chemokine expression and leukocyte infiltration following Doxo treatment. An understanding of this pathway may allow for development of intervention strategies to reduce chemotherapy-induced small intestinal damage.
methodsMice were treated with (Abx) or without (NoAbx) oral antibiotics in drinking water for four weeks and then with Doxo. Jejunal tissues were collected at various time points following Doxo treatment and stained and analyzed for apoptosis, crypt damage and restitution, and macrophage and neutrophil number. In addition, RNA expression of inflammatory markers (TNFα, IL1-β, IL-10) and cytokines (CCL2, CC7, KC) was assessed by qRT-PCR.
resultsIn NoAbx mice Doxo-induced damage was associated with rapid induction of apoptosis in jejunal crypt epithelium and an increase weight loss and crypt loss. In addition, we observed an increase in immune-modulating chemokines CCL2, CCL7 and KC and infiltration of macrophages and neutrophils. In contrast, while still positive for induction of apoptosis following Doxo treatment, Abx mice showed neither the overall weight loss nor crypt loss seen in NoAbx mice nor the increased chemokine expression and leukocyte infiltration.
conclusionEnteric bacteria play a critical role in Doxo-induced small intestinal damage and are associated with an increase in immune-modulating chemokines and cells. Manipulation of enteric bacteria or the damage pathway may allow for prevention or treatment of chemotherapy-induced small intestinal damage.
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