Eosinophils as a Biomarker in Asthma and COPD

Abstract

Asthma and COPD are two diseases related to eosinophils. But at present, we do not know with certainty how much these cells participate in these diseases, beyond that the treatment of the underlying cause produces the resolution of eosinophilia in a “reactive” way. Eosinophil-related diseases are a spectrum of systemic diseases such as Asthma and COPD in pneumology area. Under inflammatory conditions, the number of circulating eosinophils or tissues can increase dramatically, with rapid development of eosinophilia and we can obtain in a simple laboratory test. In general, the number of eosinophils in the blood can provide useful information and considering the differential diagnosis and for the subsequent test of patients presenting with eosinophilia. The treatment of eosinophilia currently in number of 300 cells in which is the criteria and the target to be treat. The best known and most used of all treatments for diseases related to eosinophils are corticosteroids, which decrease circulating and tissue eosinophils in a few hours, through mechanisms that include the direct activation of eosinophil program death. Targeted treatment against eosinophils could improve airway remodeling through mechanisms that are not fully known, and their effects on lung function are variable and decreasing symptoms in patients.

Expression of CD83 in tissue-resident regulatory T cells maintains local homeostasis and restricts effector cells in allergic asthma

“…In asthma, Th2-type cells are recruited to the site of in ammation in the lung via chemokines such as CCL17 and CCL22 [28,29], which are both upregulated in asthmatic CD83cKO mice. Lung lymphocytes from asthmatic mice exhibited an increased production of CXCL5 upon restimulation with OVA, which is associated with neutrophil recruitment, but also triggers the speci c granule content release of eosinophils [30,31]. Collectively, these data suggest that CD83-deletion renders Tregs less effective to suppress Th2 responses, leading to an exacerbated asthmatic disease.…”