Effects of diesel exhaust particle exposure on a murine model of chemical asthma

Abstract

Introduction: Ammonium persulfate (AP) is a highly reactive salt that causes occupational asthma. Diesel exhaust particles (DEP) are implicated in the increase of respiratory sensitization to allergens, but no studies have been done on the role of DEP in asthma due to chemical agents. Hereby, the present study aims to shed light on the role of DEP in asthma due to chemical exposure. Methods: BALB/c ByJ were randomly divided into four experimental groups. On days 1 and 8, received dermal applications of 5%AP or vehicle. On days 15, 18 and 21, received 1%AP or vehicle via intranasal instillation. Two experimental groups received DEP on every of the three challenges. Twenty four hours after the last intranasal instillation, the lungs were processed to characterize lung immune cells by flow citometry: T and B cells, NK, neuthophils, eosinophils, inflammatory and resident monocytes, alveolar and interstitial macrophages, CD11b- and CD11b+ dendritic cells (DC). Results: Eosinophils increased significantly after AP challenge (p=0.026) compared with the control group. DEP increased neutrophils (p=0.002), NK (p=0.008) and decreased monocytes (p=0.008). The co-exposure of AP and DEP increased eosinophils (p=0.003), NKs (p=0.024) and decreased macrophages (p=0.006), and monocytes (p=0.025). Compared with AP group, DEP and AP+DEP decreased alveolar macrophages and increased interstitial macrophages (p Conclusions: This study characterizes the immunological mechanisms underlying the exposure to DEP. The results demonstrated that DEP exposure activates the innate immune response and together with AP, exacerbates asthma immune hallmarks. Study supported by Instituto de Salud Carlos III (PI15/01900) and FEDER.