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Vagal TRPV1+ sensory neurons regulate myeloid cell dynamics and protect against influenza virus infection

ABSTRACT: Influenza viruses are a major global cause of morbidity and mortality. While vagal TRPV1+ nociceptive sensory neurons are known to mediate defenses against harmful agents, their function in lung antiviral defenses remains unclear. Our study reveals that both systemic and vagal-specific ablation of TRPV1+ nociceptors reduce survival in mice infected with influenza A virus (IAV). Despite no difference in viral load, mice lacking TRPV1+ neurons exhibited increased viral spread, exacerbated lung pathology, and elevated levels of pro-inflammatory cytokines. Loss of TRPV1+ neurons altered the lung immune landscape, including an expansion of neutrophils and monocyte-derived macrophages. Transcriptional analysis revealed impaired interferon signaling in these myeloid cells and an imbalance in distinct neutrophil sub-populations in the absence of nociceptors. Furthermore, antibody-mediated depletion of myeloid cells during IAV infection significantly improved survival, underscoring a role of TRPV1+ nociceptors in preventing pathogenic myeloid cell states that contribute to IAV-induced mortality.

ORGANISM(S): Mus musculus

PROVIDER: GSE296065 | GEO | 2025/08/01

REPOSITORIES: GEO

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