Apoptotic eosinophils in sputum from asthmatic patients correlate negatively with levels of IL-5 and eotaxin

Abstract

Apoptosis of eosinophils might be suppressed by proinflammatory cytokines and chemokines such as IL-5 and eotaxin leading to their accumulation in the lung. Stimulation of eosinophils in airway with IL-5 and eotaxin may play a crucial role in allergic inflammation.

CCL11 as a potential diagnostic marker for asthma?

“…Infiltration of eosinophils into the bronchial wall and respiratory epithelial damage are distinctive features of asthma [31]. Inhaled allergen activates mast cells and Th2 lymphocytes in the lung to generate the cytokines IL-4, IL-13 and TNF-a, which stimulates the release of CCL11 by epithelial cells, fibroblasts, endothelial cells [24,31,45,46].…”

“…Inhaled allergen activates mast cells and Th2 lymphocytes in the lung to generate the cytokines IL-4, IL-13 and TNF-a, which stimulates the release of CCL11 by epithelial cells, fibroblasts, endothelial cells [24,31,45,46]. As the most potent and selective chemoattractant for eosinophils [8,17], CCL11 can stimulate migration [32], adhesion and recruitment of eosinophils into the airways [11,47,48], in cooperation with other mediators, such as RANTES and IL-5 [49,50].…”

Inhaled Carbenoxolone Prevents Allergic Airway Inflammation and Airway Hyperreactivity in a Mouse Model of Asthma

“…IL-4 also upregulates endothelial vascular cell adhesion molecule-1 on the endothelium, which may interact with very late antigen-4 on eosinophils and promotes their eosinophil recruitment into the airways [24]. IL-5 is one of the key cytokines responsible for maturation, growth and recruitment of eosinophils, and it also promotes the chronic presence of eosinophils in the airways by reducing their apoptosis [25]. The treatment of CBX markedly attenuated the levels of IL-4, IL-5 and IgE.…”

Mepacrine alleviates airway hyperresponsiveness and airway inflammation in a mouse model of asthma

“…These findings indicate that mepacrine could be involved in the reduction of BAL fluid eosinophils and IgE levels by decreasing the expression of adhesion molecules and altering IgE class switching. IL-5 is one of the key cytokines responsible for maturation, growth and recruitment of eosinophils and it also promotes the chronic presence of eosinophils in the airway by reducing their apoptosis [29]. IL-13 also has a pivotal role in causing crucial features of asthma such as airway hyperresponsiveness, airway inflammation, increased IgE synthesis, mucus metaplasia and subepithelial fibrosis [30].…”