Obesity alters the lung myeloid cell landscape to enhance breast cancer metastasis through IL5 and GM-CSF
Open accessAbstract
Obesity is associated with chronic, low-grade inflammation, which can disrupt homeostasis within tissue microenvironments. Given the correlation between obesity and relative risk of death from cancer, we investigated whether obesity-associated inflammation promotes metastatic progression. We demonstrate that obesity causes lung neutrophilia in otherwise normal mice, which is further exacerbated by the presence of a primary tumour. The increase in lung neutrophils translates to increased breast cancer metastasis to this site, in a GM-CSF- and IL5-dependent manner. Importantly, weight loss is sufficient to reverse this effect, and reduce serum levels of GM-CSF and IL5 in both mouse models and humans. Our data indicate that special consideration of the obese patient population is critical for effective management of cancer progression.
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The direct use of specific diets, or the modulation of inter‐organ communication, could have a pharmacological effect on its own or increase the efficiency of pharmacological approaches.
“Therefore, the direct use of specific diets, or the modulation of inter‐organ communication, could have a pharmacological effect on its own 167 or increase the efficiency of pharmacological approaches to treat a wide variety of diseases 173, 174.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [174]
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References 72 · Cited by 277
- Authors
- Quail, D. F., Olson, O. C., Bhardwaj, P., Walsh, L. A., Akkari, L., Quick, M. L., Chen, I.-C., Wendel, N., Ben-Chetrit, N., Walker, J., Holt, P. R., Dannenberg, A. J., & Joyce, J. A.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Weill Cornell Medicine (US)
- Rockefeller University (US)
- Corresponding author
- Joyce, Johanna A.
- ORCID
- Venue
- Nature Cell Biology
- Published
- 2017-07-24
- Volume
- 19
- Issue
- 8
- Pages
- 974-987
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- PMC
- PMC6759922
- OpenAlex
- W2737206084
- Cited by
- 277
- References
- 72
- Citations by year
- 2026: 18 · 2025: 33 · 2024: 24 · 2023: 43 · 2022: 25 · 2021: 44 · 2020: 37 · 2019: 24 · 2018: 24 · 2017: 5
- FWCI
- 11.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IRIS (submittedVersion)
- SERVAL (Université de Lausanne) (submittedVersion)
- Funders
- National Institutes of Health (UL1TR000043)
- National Cancer Institute (F31CA171384, U54CA210184, P30CA008748)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- obesity, breast cancer metastasis, lung metastasis, GM-CSF, IL-5, myeloid cells, chronic inflammation, weight loss, tumor microenvironment
- MeSH terms
- Animals, Breast Neoplasms, Disease Models, Animal, Female, Lung, Lung Neoplasms, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Neutrophils, Obesity, Pneumonia, Time Factors, Signal Transduction, Weight Loss, Interleukin-5, Gene Expression Regulation, Neoplastic, Granulocyte-Macrophage Colony-Stimulating Factor, Mice, SCID, Mice, Inbred NOD, Disease Progression, Diet, Fat-Restricted, Coculture Techniques, Adoptive Transfer, Neutrophil Infiltration, Cell Line, Tumor, Adiposity, Tumor Microenvironment
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