Eosinophils in the Spotlight: Eosinophilic airway inflammation in nonallergic asthma

Allergen-Induced Asthmatic Responses Modified by a GATA3-Specific DNAzyme

“…35,36 This type-2 endotype not only is present in prototypical atopic and allergic asthma but also has recently been observed in other clinical phenotypes of asthma, including hypereosinophilic late-onset asthma, persistent and severe asthma, and aspirin-sensitive asthma. 5,37,38 The criteria for inclusion in the study were designed to cover a broad spectrum of patients with this endotype (e.g., requiring only the "presence of sputum eosinophils"), and the data on lung function showed that SB010 had a significant effect in this population. SB010 had a more pronounced attenuating effect on the late asthmatic response, but there was also significant attenuation in the early asthmatic response.…”

The PPARγ agonist, rosiglitazone, attenuates airway inflammation and remodeling via heme oxygenase-1 in murine model of asthma

“…Airway inflammation and remodeling are the two characterized pathological [15,16] . Among the inflammatory cells participated in occurrence and development of asthma, eosinophils play a featured role [17,18] . It was considered that the inflammatory mediators and cytokines released by accumulated eosinophils in airway resulted in mucus hypersecretion, increased vascular permeability, bronchial hyperresponsiveness, smooth muscle contraction [19,20] .…”

Improving the diagnosis of eosinophilic asthma

“…Apparently, the molecular pathways leading to increased FeNO levels differ from those regulating eosinophil recruitment and activation. Increased FeNO seems to be primarily related to pathways involved in Th2-mediated asthma, whereas blood eosinophils may relate more to type 2 innate lymphoid cell (ILC2)-mediated (severe) asthma [36,37].…”

“…In allergic eosinophilic asthma, Th2 cells are driving the pathobiology of the disease, but there is accumulating evidence that in adult-onset nonallergic eosinophilic asthma, ILC2s may play a more prominent role [36]. Air pollutants, microbes, and glycolipids induce the release of epitheliumderived cytokines that activate ILC2s, which are then able to produce high amounts of IL-5 and IL-13 leading to eosinophilia [82,83].…”

“…ILC2s are present in greater numbers in sputum and blood of patients with severe eosinophilic asthma compared to mild allergic asthmatics and produce high levels of IL-5 and IL-13 in sputum [84]. Thus, ILC2s and its cytokines can promote the persistence of airway eosinophilia independent of allergen exposure, which explains the lack of response of anti-IL-5 in the allergen challenge model, and the presence of eosinophilic inflammation in nonallergic asthma [36]. Because of the close association between ILC2s in peripheral blood and sputum eosinophils, ILC2s have even been proposed as novel biomarkers for eosinophilic asthma [85].…”