AI Article Synopsis
- Human lung squamous cell carcinoma (SCC) is linked to increased infiltration of specific macrophages that express high levels of inducible nitric oxide synthase (NOS2).
- Research showed that when NOS2 is absent, there are fewer macrophages, reduced lung fibrosis, and lower incidence of SCC in mice.
- The study reveals that NOS2 enhances inflammation and macrophage activity while negatively affecting lipid metabolism, contributing to the development of lung SCC.
Article Abstract
Human lung squamous cell carcinoma (SCC) is highly associated with increased pulmonary macrophage infiltration. Previously, we showed that marked pulmonary infiltrating macrophages were required for spontaneous lung SCC development in a mouse model ( , ) that resembles human lung SCC. Interestingly the lung SCC-associated macrophages specifically express elevated inducible nitric oxide synthase (NOS2). However, the role of macrophage NOS2 in lung carcinogenesis has not been explored. Here, we show that NOS2 ablation inhibits macrophage infiltration, fibrosis, and SCC development in the lungs of mice. Macrophage NOS2 was found to circulate inflammation and enhance macrophage migration and survival. NOS2 promotes foamy macrophage formation characterized with impaired lipid metabolism. NOS2 null bone marrow transplantation reduces foamy macrophage numbers and carcinogenesis in chimaeras. This finding sheds light on a new mechanism by which macrophage NOS2 increases pulmonary inflammatory responses and macrophage survival and impairs macrophage lipid metabolism, thereby promoting lung SCC formation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5967330 | PMC |
| http://dx.doi.org/10.1038/s41420-018-0046-5 | DOI Listing |
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