Gastrointestinal Tract Dysbiosis Enhances Distal Tumor Progression through Suppression of Leukocyte Trafficking
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Abstract
Abstract The overall use of antibiotics has increased significantly in recent years. Besides fighting infections, antibiotics also alter the gut microbiota. Commensal bacteria in the gastrointestinal tract are crucial to maintain immune homeostasis, and microbial imbalance or dysbiosis affects disease susceptibility and progression. We hypothesized that antibiotic-induced dysbiosis of the gut microbiota would suppress cytokine profiles in the host, thereby leading to changes in the tumor microenvironment. The induced dysbiosis was characterized by alterations in bacterial abundance, composition, and diversity in our animal models. On the host side, antibiotic-induced dysbiosis caused elongated small intestines and ceca, and B16-F10 melanoma and Lewis lung carcinoma progressed more quickly than in control mice. Mechanistic studies revealed that this progression was mediated by suppressed TNFα levels, both locally and systemically, resulting in reduced expression of tumor endothelial adhesion molecules, particularly intercellular adhesion molecule-1 (ICAM-1) and a subsequent decrease in the number of activated and effector CD8+ T cells in the tumor. However, suppression of ICAM-1 or its binding site, the alpha subunit of lymphocyte function-associated antigen-1, was not seen in the spleen or thymus during dysbiosis. TNFα supplementation in dysbiotic mice was able to increase ICAM-1 expression and leukocyte trafficking into the tumor. Overall, these results demonstrate the importance of commensal bacteria in supporting anticancer immune surveillance, define an important role of tumor endothelial cells within this process, and suggest adverse consequences of antibiotics on cancer control. Significance: Antibiotic-induced dysbiosis enhances distal tumor progression by altering host cytokine levels, resulting in suppression of tumor endothelial adhesion molecules and activated and effector CD8+ T cells in the tumor.
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As a consequence of antibiotics-induced dysbiosis, the number of activated CD8+ T cells decreased.
“As a consequence, the number of activated CD8+T cells decreased [37].”
From Gut microbiota-mediated immunomodulation in tumor (2021) · cites this paper as [37]
Antibiotics-induced dysbiosis promoted tumor growth via a suppressed level of TNF-α and a subsequent decrease in tumor endothelial adhesion molecules, especially intercellular adhesion molecule 1 (ICAM-1).
“In contrast, antibiotics-induced dysbiosis promoted tumor growth via a suppressed level of TNF-α and a subsequent decrease in tumor endothelial adhesion molecules, especially intercellular adhesion molecule 1 (ICAM-1).”
From Gut microbiota-mediated immunomodulation in tumor (2021) · cites this paper as [37]
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Kanser Gelişiminde ve Tedavisinde Mikrobiyotanın Rolü
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Harnessing the immune system in lung cancer: emerging role of the microbiome
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Microbiota and metabolites modulation of cancer stem cells and chemotherapy sensitivity
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- Authors
- Jenkins, S. V., Robeson, M. S., Griffin, R. J., Quick, C. M., Siegel, E. R., Cannon, M. J., Vang, K. B., & Dings, R. P. M.
- Affiliations
- University of Arkansas for Medical Sciences (US)
- University of Arkansas at Little Rock (US)
- Corresponding author
- Dings, Ruud P.M.
- ORCID
- Venue
- Cancer Research
- Published
- 2019-12-01
- Volume
- 79
- Issue
- 23
- Pages
- 5999-6009
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC6891208
- OpenAlex
- W2978260485
- Cited by
- 41
- References
- 49
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 5 · 2023: 8 · 2022: 3 · 2021: 12 · 2020: 3
- FWCI
- 1.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- HHS | NIH | National Institute of General Medical Sciences (P20GM103625)
- National Science Foundation (OIA-1457888)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biotechnology › Cancer Research and Treatments
- Keywords
- gut dysbiosis, antibiotic-induced dysbiosis, leukocyte migration, TNF-α, ICAM-1, LFA-1, tumor endothelial cells, CD8+ T cells, tumor microenvironment, B16F10 melanoma, Lewis lung carcinoma, commensal bacteria, cytokine profile
- MeSH terms
- Gastrointestinal Microbiome, Animals, Anti-Bacterial Agents, Endothelium, Melanoma, Experimental, Tumor Necrosis Factor-alpha, Lymphocytes, Tumor-Infiltrating, CD8-Positive T-Lymphocytes, Disease Progression, Intercellular Adhesion Molecule-1, Carcinoma, Lewis Lung, Mice, Dysbiosis
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