Studies for the adverse effects of environmental nanoparticles on sensitive pulmonary diseases

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In reality, we inhale suspended DEP and/or nanoparticles in ambient air Nevertheless, assessment of the impact of inhalation/intratracheal exposure to diesel engine-derived nanoparticles, a more realistic exposure, on the lung inflammation model has never been conducted. Furthermore, as far as we know, no study has examined the dose-dependent effects of inhaled nanoparticles on predisposed subjects. The present study investigated the impact of pulmonary exposure to diesel-engine-derived nanoparticles on emphysematous lung injury and allergic airway inflammation and dissolved its underlying mechanisms. In the first experiments, CBNP of 14 nm significantly induced acute lung inflammation in non-elicited subjects, and aggravated PPE-elicited airway neutrophilic inflammation at an early stage, which was concomitant with the enhanced lung expression of proinflammatory cytokines. In the next experiments, high concentration of NR-DE significantly deteriorated OVA-induced eosinophilic airway inflammation. On the other hand, DE gas did not influence PPE-induced pulmonary inflammation with emphysema. In in vitro experiments, NR-DEP significantly enhanced mucin-1 expression on BEAS-2B cells and surface expression of CD86 on mouse-derived splenocytes and dendritic cells.