ArticlePloS one2015
The Adaptor Protein Myd88 Is a Key Signaling Molecule in the Pathogenesis of Irinotecan-Induced Intestinal Mucositis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- Mechanisms and therapeutic potential of therapy-induced cellular senescence in radiotherapy- and chemotherapy-related alimentary tract mucositis.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026Review
- A Comprehensive Review on Irinotecan-Induced Delayed Diarrhea: From Mechanisms to Therapeutic Options.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The mucosal-neural axis in chemotherapy-induced gastrointestinal toxicity.Oncology reviews · 2026Review
- Spermidine protects against ETEC-induced intestinal injury by reshaping the gut microbiota and activating the AhR/IL-22 axis.Frontiers in microbiology · 2026Article
- Intestinal Goblet Cell-Expressed Reg4 Ameliorates Intestinal Inflammation Potentially by Restraining Pathogenic Escherichia coli Infection.Probiotics and antimicrobial proteins · 2025Article
- Gut-Protective and Multifunctional Exopolysaccharide fromNutrients · 2025Article
- Gold nanoparticles as innovative therapeutics for oral mucositis: A review of current evidence.Drug delivery and translational research · 2025Review
- Baihu Guizhi decoction alleviates inflammation in rats with acute gouty arthritis by targeting miR-17-5p to regulate the TLR4/Myd88/NF-κB signaling pathway.Clinics (Sao Paulo, Brazil) · 2025Article
- The microbiota in breast cancer: dysbiosis, microbial metabolites, and therapeutic implications.American journal of cancer research · 2025Review
- Is There an Interplay between Environmental Factors, Microbiota Imbalance, and Cancer Chemotherapy-Associated Intestinal Mucositis?Pharmaceuticals (Basel, Switzerland) · 2024Article
- Incomplete Knockdown of MyD88 Inhibits LPS-Induced Lung Injury and Lung Fibrosis in a Mouse Model.Inflammation · 2023Article
- Therapeutic effects of a lipid transfer protein isolated from Morinda citrifolia L. (noni) seeds on irinotecan-induced intestinal mucositis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Decreased Tissue Omega-6/Omega-3 Fatty Acid Ratio Prevents Chemotherapy-Induced Gastrointestinal Toxicity Associated with Alterations of Gut Microbiome.International journal of molecular sciences · 2022Article
- The science of mucositis.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2022Article
- Roles of Toll-Like Receptors in Radiotherapy- and Chemotherapy-Induced Oral Mucositis: A Concise Review.Frontiers in cellular and infection microbiology · 2022Review
- Chemotherapy-Induced Intestinal Microbiota Dysbiosis Impairs Mucosal Homeostasis by Modulating Toll-like Receptor Signaling Pathways.International journal of molecular sciences · 2021Review
- Gut Microbiota: A Potential Target for Cancer Interventions.Cancer management and research · 2021Review
- Breast and Gut Microbiota Action Mechanisms in Breast Cancer Pathogenesis and Treatment.Cancers · 2020Review
- Troxerutin Prevents 5-Fluorouracil Induced Morphological Changes in the Intestinal Mucosa: Role of Cyclooxygenase-2 Pathway.Pharmaceuticals (Basel, Switzerland) · 2020Article
- EnteropathogenicFrontiers in cellular and infection microbiology · 2020Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intestinal mucositis is a common side effect of irinotecan-based anticancer regimens. Mucositis causes cell damage, bacterial/endotoxin translocation and production of cytokines including IL-1 and IL-18. These molecules and toll-like receptors (TLRs) activate a common signaling pathway that involves the Myeloid Differentiation adaptor protein, MyD88, whose role in intestinal mucositis is unknown. Then, we evaluated the involvement of TLRs and MyD88 in the pathogenesis of irinotecan-induced intestinal mucositis. MyD88-, TLR2- or TLR9-knockout mice and C57BL/6 (WT) mice were given either saline or irinotecan (75 mg/kg, i.p. for 4 days). On day 7, animal survival, diarrhea and bacteremia were assessed, and following euthanasia, samples of the ileum were obtained for morphometric analysis, myeloperoxidase (MPO) assay and measurement of pro-inflammatory markers. Irinotecan reduced the animal survival (50%) and induced a pronounced diarrhea, increased bacteremia, neutrophil accumulation in the intestinal tissue, intestinal damage and more than twofold increased expression of MyD88 (200%), TLR9 (400%), TRAF6 (236%), IL-1β (405%), IL-18 (365%), COX-2 (2,777%) and NF-κB (245%) in the WT animals when compared with saline-injected group (P<0.05). Genetic deletion of MyD88, TLR2 or TLR9 effectively controlled the signs of intestinal injury when compared with irinotecan-administered WT controls (P<0.05). In contrast to the MyD88-/- and TLR2-/- mice, the irinotecan-injected TLR9-/- mice showed a reduced survival, a marked diarrhea and an enhanced expression of IL-18 versus irinotecan-injected WT controls. Additionally, the expression of MyD88 was reduced in the TLR2-/- or TLR9-/- mice. This study shows a critical role of the MyD88-mediated TLR2 and TLR9 signaling in the pathogenesis of irinotecan-induced intestinal mucositis.
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