2026-01-19 イェール大学
Electron micrograph showing a human nasal epithelial cell releasing rhinovirus (blue). Credit: Julien Amat, Bao Wang
<関連情報>
- https://news.yale.edu/2026/01/19/why-same-cold-can-be-sniffle-some-and-crisis-others
- https://www.cell.com/cell-press-blue/fulltext/S3051-3839(25)00001-5
ライノウイルスは上皮細胞の自然免疫シグナル伝達の異なる関与を通じて異なる宿主反応を引き起こす Rhinovirus triggers distinct host responses through differential engagement of epithelial innate immune signaling
Bao Wang ∙ Julien A.R. Amat ∙ Valia T. Mihaylova ∙ Yong Kong ∙ Guilin Wang ∙ Ellen F. Foxman
Cell Pres Blue Published:January 19, 2026
DOI:https://doi.org/10.1016/j.cpblue.2025.100001
Highlights
- Nasal epithelial organoids capture a spectrum of responses to rhinovirus infection
- Blocking interferon response leads to IL-1β release and mucus hyperproduction
- Targeting NLRP1 alleviates the inflammatory response to rhinovirus
Summary
Rhinoviruses (RVs) are the most frequent cause of common colds, but they are also a major cause of respiratory distress in high-risk groups (e.g., smokers and people with asthma). The molecular mechanisms leading to the wide range of infection outcomes are not fully understood. Using single-cell sequencing of an organotypic model of the human nasal epithelium and mechanistic experiments, here we show that differential engagement of innate immune signaling pathways alters the inflammatory response initiated in RV target cells. In the intact human nasal epithelium, RV primarily induces an interferon response, which restricts the infection to <2% of cells. Inhibiting this response increases viral replication and exaggerates nuclear factor κB (NF-κB)- and Nod-like receptor protein 1 (NLRP1)-dependent pro-inflammatory responses and mucus hyperproduction with positive feedback from interleukin (IL)-1β release. These results elucidate molecular mechanisms leading to distinct host responses to RV infection and reveal potential therapeutic targets.
