Annually, 6,5 million people die from breathing unhealthy air, making air pollution a major threat not only to climate change but also human health. The World Health Organization (WHO) states that 99% of the world population is exposed to air pollution that exceeds WHO guideline levels (annual mean concentrations of PM2.5<5 µg/m3, NO2<10 µg/m3 and ozone<60 µg/m3) and could therefore have a negative impact on human health. Studies have confirmed the influence of air pollutants, such as diesel exhaust particles (DEPs), on the onset and exacerbation of asthma. However, mechanisms used by DEPs to induce or exacerbate asthma remain largely unknown. In this thesis, we aim to characterize the aggravating effects of DEPs on allergic asthma. Therefore, our lab established a murine model, in which house dust mite (HDM) and DEP are concomitantly administered. Using this model, we characterized neutrophilic responses in type 2 inflammation by looking at chemokines and neutrophil mediators. Additionally, the role of the neutrophil in this inflammation was investigated through inhibition of a neutrophil mediator and neutrophil depletion experiments. Acute inflammation was characterized in an acute model of pollutant-aggravated asthma. Inflammatory cell infiltration was investigated by performing analyses at 2 time points. With this research, we hope to provide new knowledge on pollutant-aggravated inflammation in allergic asthma. Our model allows to determine how exposure to air pollution can influence the response to current asthma therapy. Additionally, new or repurposing therapies could be considered for asthma patients, suffering from pollutant-induced exacerbations. The neutrophil elastase inhibitor Sivelestat is currently tested for acute respiratory distress syndrome (ARDS), but could be contemplated for drug repurposing in asthma patients, when shown to be promising in our murine model.