Non-Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock


Mild dyslipidemia accelerates tumorigenesis through expansion of Ly6Chi monocytes and differentiation to pro-angiogenic myeloid cells.


Cancer and cardiovascular disease (CVD) share common risk factors such as dyslipidemia, obesity and inflammation. However, the role of pro-atherogenic environment and its associated low-grade inflammation in tumor progression remains underexplored. Here we show that feeding C57BL/6J mice with a non-obesogenic high fat high cholesterol diet (HFHCD) for two weeks to induce mild dyslipidemia, increases the pool of circulating Ly6Chi monocytes available for initial melanoma development, in an IL-1beta-dependent manner. Descendants of circulating myeloid cells, which accumulate in the tumor microenvironment of mice under HFHCD, heighten pro-angiogenic and immunosuppressive activities locally. Limiting myeloid cell accumulation or targeting VEGF-A production by myeloid cells decrease HFHCD-induced tumor growth acceleration. Reverting the HFHCD to a chow diet at the time of tumor implantation protects against tumor growth. Together, these data shed light on cross-disease communication between cardiovascular pathologies and cancer.

Authors: Tran T, Lavillegrand JR, Lereverend C, Esposito B, Cartier L, Montabord M, Tran-Rajau J, Diedisheim M, Gruel N, Ouguerram K, Paolini L, Lenoir O, Pinteaux E, Brabencova E, Tanchot C, Urquia P, Lehmann-Che J, Le Naour R, Merrouche Y, Stockmann C, Mallat Z,
Journal: Nat Commun;2022Sep14; 13 (1) 5399. doi:10.1038/s41467-022-33034-0
Year: 2022
PubMed: PMID: 36104342 (Go to PubMed)