{Reference Type}: Journal Article
{Title}: Non-allergic eosinophilic inflammation and airway hyperresponsiveness induced by diesel engine exhaust through activating ILCs.
{Author}: Zhao H;Zhan C;Li B;Fang Z;Zhong M;He Y;Chen F;Chen Z;Zhang G;Zhong N;Lai K;Chen R;
{Journal}: Ecotoxicol Environ Saf
{Volume}: 278
{Issue}: 0
{Year}: 2024 Jun 15
{Factor}: 7.129
{DOI}: 10.1016/j.ecoenv.2024.116403
{Abstract}: <B>BACKGROUND: </B>Diesel engine exhaust (DEE) is associated with the development and exacerbation of asthma. Studies have shown that DEE can aggravate allergen-induced eosinophilic inflammation in lung. However, it remains not clear that whether DEE alone could initiate non-allergic eosinophilic inflammation and airway hyperresponsiveness (AHR) through innate lymphoid cells (ILCs) pathway.<BR><B>OBJECTIVE: </B>This study aims to investigate the airway inflammation and hyperresponsiveness and its relationship with ILC after DEE exposure.<BR><B>METHODS: </B>Non-sensitized BALB/c mice were exposed in the chamber of diesel exhaust or filtered air for 2, 4, and 6 weeks (4 h/day, 6 days/week). Anti-CD4 mAb or anti-Thy1.2 mAb was administered by intraperitoneal injection to inhibit CD4+T or ILCs respectively. AHR、airway inflammation and ILCs were assessed.<BR><B>RESULTS: </B>DEE exposure induced significantly elevated level of neutrophils, eosinophils, collagen content at 4, 6 weeks. Importantly, the airway AHR was only significant in the 4weeks-DEE exposure group. No difference of the functional proportions of Th2 cells was found between exposure group and control group. The proportions of IL-5+ILC2, IL-17+ILC significantly increased in 2, 4weeks-DEE exposure group. After depletion of CD4+T cells, both the proportion of IL-5+ILC2 and IL-17A ILCs was higher in the 4weeks-DEE exposure group which induced AHR, neutrophilic and eosinophilic inflammation accompanied by the IL-5, IL-17A levels.<BR><B>CONCLUSIONS: </B>Diesel engine exhaust alone can imitate asthmatic characteristics in mice model. Lung-resident ILCs are one of the major effectors cells responsible for a mixed Th2/Th17 response and AHR.