Enrichment of the lungs with oral commensal microbes was associated with advanced stage disease, worse prognosis, and tumor progression in patients with lung cancer, according to results from a study published in Cancer Discovery, a journal of the American Association for Cancer Research.

Scientists of the he Lung Microbiome Program at the New York University Grossman School of Medicine and of NYU Langone’s Perlmutter Cancer Center analyzed the lung microbiomes of 83 untreated adult patients with lung cancer using samples obtained from diagnostic clinical bronchoscopies. Samples were analyzed to identify microbial composition and to determine which genes were expressed in lung tissue.

The researchers found that patients who had advanced-stage lung cancer (stages 3b-4) had greater enrichment of oral commensals in the lung than those who had early-stage disease (stages 1-3a). Furthermore, the enrichment of oral commensals in the lung was associated with decreased survival, even after adjusting for tumor stage. Poor prognosis was
associated with the enrichment of Veillonella, Prevotella, and Streptococcus bacteria in the lung microbiome, and tumor progression was associated with the enrichment of Veillonella, Prevotella, Streptococcus,
and Rothia bacteria.

In patients with early-stage disease, enrichment of Veillonella, Prevotella, and Streptococcus was associated with activation of the p53, PI3K/PTEN, ERK, and IL-6/IL-8 signaling pathways. A Veillonella strain,found to be enriched in patients with advanced-stage lung cancer, was associated with the expression of IL-17, cell adhesion molecules,
cytokines, and growth factors, as well as with the activation of the TNF, PI3K-AKT, and JAK-STAT signaling pathways.

The team also examined the effects of the lung microbiome in a mouse model of lung cancer. They seeded Veillonella parvula in the lungs of mice with lung cancer to model the enrichment of oral commensals. This led to decreased survival, weight loss, and increased tumor burden and was associated with increased expression of IL-17 and other inflammatory proteins, increased recruitment of immune-suppressing cells, and increased activation of inflammatory pathways. To understand the role of IL-17 in lung cancer pathogenesis, the team tried mice with an antibody targeted to
IL-17, which resulted in a significant decrease in tumor burden compared to mice treated with a control.

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