Silica and double-stranded RNA synergistically induce bronchial epithelial apoptosis and airway inflammation

Hirotoshi Unno, Kyoko Futamura, Hideaki Morita, Reiji Kojima, Ken Arae, Susumu Nakae, Hiroyuki Ida, Hirohisa Saito, Kenji Matsumoto, Akio Matsuda

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


Silica crystals (silica), which are the main mineral component of volcanic ash and desert dust, can activate the caspase-1-activating inflammasome in phagocytic cells to secrete IL-1β. Although inhalation of silica-containing dust is known to exacerbate chronic respiratory diseases, probably through inflammasome activation, its direct effects on bronchial epithelial cells remain unclear. Here, we show that silica and double-stranded RNA (dsRNA) synergistically induces caspase-9-dependent apoptosis, but not inflammasome activation, of bronchial epithelial cells. Intranasal administration of silica and dsRNA to mice synergistically enhanced neutrophil infiltration in the airway without IL-1β release in the bronchoalveolar lavage fluid. Histopathological analysis revealed that silica or dsRNA alone induced slight airway inflammation, whereas combined administration significantly enhanced airway inflammation and epithelial damage. These novel findings suggest that inhalation of silica-containing dust may cause inflammasome-independent airway inflammation, possibly by damaging the epithelial barrier, especially at the time of viral infection. These responses may also be involved in acute lung injury caused by inhaled silica-containing dust.

Original languageEnglish
Pages (from-to)344-353
Number of pages10
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Issue number3
Publication statusPublished - 09-2014
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology


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