Asian sand dust enhances rhinovirus-induced cytokine secretion and viral replication in human nasal epithelial cells.
Asian sand dust (ASD) originating in the arid deserts of Mongolia and China causes annual severe air pollution events in the Asia-Pacific area, including Korea, Japan, and China. ASD is thought to impact public health by aggravating or inducing respiratory illness. Among the most common respiratory illnesses is the common cold caused by rhinovirus (RV) infection. To date, however, the impact of ASD on RV infection has not been studied. In this study, we investigated the effect of ASD on RV infection in human nasal epithelial cells. Primary human nasal epithelial cells grown at an air-liquid interface were treated with ASD and/or RV. After RV infections were confirmed using semi-nested reverse transcription-polymerase chain reaction (RT-PCR), mRNA expression and protein secretion of the inflammatory cytokines interferon-γ (IFN-γ), interleukin-1β (IL-1β),IL-6, and IL-8, indicators of the severity of RV-induced inflammation, were measured by real-time PCR and enzyme-linked immunosorbent assays. Viral titer was also assayed by culturing viruses to compare viral replication between RV-only and ASD-plus-RV groups. ASD significantly increased RV-induced IFN-γ, IL-1β, IL-6, and IL-8 mRNA levels and protein secretion in primary nasal epithelial cells. In addition, ASD caused a significant increase in RV replication. Our results suggest that ASD may potentiate common cold symptoms associated with RV infection not only by enhancing IFN-γ, IL-1β, IL-6, and IL-8 secretion, but also by increasing viral replication.