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Respiratory viral infections prime accelerated lung cancer growth [scRNA-Seq]

ABSTRACT: The COVID-19 pandemic has highlighted long-term health consequences of viral pneumonia, yet its impact on cancer development and progression remains poorly understood. Here, we show that prior SARS-CoV-2 or influenza infection accelerates lung tumor progression by reprogramming the local immune landscape. To define mechanisms underlying infection-induced tumor promotion, we performed single-cell RNA-seq on whole-lung cells from KP mice at 6 weeks (PBS_T6, IAV_T6) and 12 weeks (PBS_T12, IAV_T12) after tumor induction, along with tumor-free PBS and IAV controls (time matched to T6). Across conditions, scRNA-seq revealed that prior viral pneumonia programs a pro-tumor lung microenvironment marked by increased pro-tumor myeloid programs and diminished anti-tumor CD8+ T cell immunity. Notably, we identified a dominant SiglecF^hi tumor-associated neutrophil subset enriched in infected tumors that exhibits hypoxia/glycolysis- and immunosuppression-associated transcriptional programs and shows the strongest predicted interactions with progenitor and tumor epithelial populations.

ORGANISM(S): Mus musculus

PROVIDER: GSE317576 | GEO | 2026/01/27

REPOSITORIES: GEO

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Project description:Vaccination reduces morbidity and mortality from pneumonia but its effect on the tissue-level response to infection is still poorly understood. We evaluated pneumonia disease progression, acute phase response and lung gene expression profiles in mice inoculated intranasally with virulent gram-positive Streptococcus pneumoniae serotype (ST) 3, with and without prior immunization with pneumococcal polysaccharide ST 3 (PPS3), or co-immunization with PPS3 and with a low dose of lipopolysaccharide (LPS). Pneumonia severity was assessed in the acute phase, 5, 12, 24 and 48 h post-inoculation (p.i.) and the resolution phase of 7 days p.i. Primary PPS3 specific antibody production was upregulated and IgM binding to pneumococci increased in PPS3-immunized mice. Immunizations with PPS3 or PPS3 + LPS decreased bacterial recovery the lung and blood at 24 and 48 h and increased survival. Microarray analysis of whole lung RNA revealed significant changes in the acute phase protein serum amyloid A (SAA) between noninfected and infected mice, which were attenuated by immunization. SAA transcripts were higher in the liver and lungs of infected controls, and SAA protein was elevated in serum, but decreased in PPS3-immunized mice. Thus, during a virulent pneumonia infection, prior immunization with PPS3 in an IgM-dependent manner as well as co-immunization with PPS3 + LPS attenuated pneumonia severity and promoted resolution of infection, concomitant with significant regulation of cytokine gene expression in the lungs, and acute phase proteins in the lungs, liver and serum. Each lung RNA sample represented an individual mouse, creating biological repeats for each treatment. In-vivo treatments were as follows: non-infected lung (vehicle-immunized) control (n=5), infected lung (vehicle-immunized) control at 48 hr post-inoculation (n=5), PPS3 and LPS co-immunized lung at 48 hr post-inoculation (n=4) and PPS3 and LPS co-immunized lung at 7 days post-inoculation (n=4).

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Respiratory viral infections prime accelerated lung cancer growth [scRNA-Seq]

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