Identification of Activated T Lymphocytes and Eosinophils in Bronchial Biopsies in Stable Atopic Asthma

Abstract

We have used immunohistochemistry and monoclonal antibodies to analyze the phenotypic composition and activation status of the cellular infiltrate of bronchial biopsies obtained by fiber optic bronchoscopy of 11 atopic asthmatic subjects (FEV1% predicted range 78 to 114), 9 atopic nonasthmatic control subjects, and 10 normal healthy subjects. Examination of mucosal biopsies obtained from both central (level I) and subsegmental (level II) bronchi showed that the highest number of CD45-, DC3-, DC4-, and CD8-positive cells were found in the group with asthma. There was a significant increase in the number of interleukin-2 receptor (CD25)-positive cells (a marker of lymphocyte activation) at airway level I in the asthmatic group compared with both nonasthmatic atopic (p less than 0.05) and normal control subjects (p less than 0.01). Eosinophil numbers were significantly increased in asthma at both airway levels and at airway level II in the nonasthmatic atopic group when compared with normal healthy control subjects (p less than 0.05). EG2-positive cells (an index of secretion of eosinophil cationic protein following activation) were found at both airway levels in the asthmatic group and at level I in the nonasthmatic atopic control group (p less than 0.05). When asthmatic subjects were compared with normal healthy subjects, there was a reduction in the number of neutrophil elastase-positive cells in the asthmatic subjects which, as a percentage of leukocytes, was significant (p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

A single administration of interleukin-4 antagonistic mutant DNA inhibits allergic airway inflammation in a mouse model of asthma

“…In the case of allergic asthma, the airway wall is infiltrated by Th2 cells, eosinophils and mast cells, [28][29][30][31] and AHR is considered to be the result of a combination of submucosal edema, infiltration of the airway epithelium by eosinophils and lymphocytes, damage to epithelial cells, and direct effect of mediators derived from mast cells and eosinophils. The occurrence of these phenomena has been confirmed in murine models in which Th2-type immune responses were induced.…”

Cytokine gene-modulated dendritic cells protect against allergic airway inflammation by inducing IL-10+IFN-γ+CD4+ T cells

“…It is recognized that CD4 + T-helper type 2 (Th2) cells and their cytokines (interleukin (IL)-4, IL-5, and IL-13) are responsible for initiating and maintaining allergic disorders. 1,2 Numerous studies indicated that regulating asthma and allergic diseases is complex, involving several different mechanisms and cell types, and might not be reflected in a simple, dichotomous balance of polarized cells, as suggested by the T-helper type 1 (Th1)/Th2 paradigm. 3,4 Dendritic cells (DCs), as professional antigen-presenting cells, have an important function in antigen presentation in the airways, and the cytokine profile secreted by DCs can influence differentiation of T cells.…”

Allergen‐induced inflammation and airway epithelial and smooth muscle cell proliferation: role of Jun N‐terminal kinase

“…Asthma is characterised by a chronic inflammatory process, consisting of eosinophils, lymphocytes and macrophages together with bronchial hyper-responsiveness (BHR) (Azzawi et al, 1990;Bousquet et al, 1990;Djukanovic et al, 1990;Bradley et al, 1991). One of the consequences of chronic airway inflammation in asthma is remodelling of the airways, which consists of increases in airway smooth muscle (ASM) mass (Dunnill et al, 1969), goblet cell hyperplasia (Laitinen et al, 1985;Aikawa, 2001) and subepithelial fibrosis (Roche et al, 1989).…”