title: Inflammation and structural changes in the airways of patients with atopic and nonatopic asthma. BHR Group.
abstract: The aim of the present study was to compare the cellular pattern and structural changes in the airway walls of atopic and nonatopic patients with asthma. Bronchial biopsy specimens were obtained from 13 atopic subjects with asthma, nine nonatopic patients with asthma, and seven healthy control subjects and investigated using immunohistochemical methods. The number of eosinophils increased in both asthma groups, but significantly more in the atopic group. The number of mast cells increased similarly in the two asthma groups, whereas the number of neutrophils increased only in the nonatopic asthma group. The number of T-lymphocytes (CD3-, CD4-, CD8-, CD-25-positive cells) was higher in patients with atopic asthma compared with nonatopic asthma. Interleukin-4 (IL-4) and IL-5-positive cells were more frequently found in the atopic asthma group, whereas cells staining for IL-8 were more frequent in the nonatopic group. The degree of epithelial damage was significantly higher in the atopic asthma group compared with the control subjects and the nonatopic asthmatics. The tenascin and laminin layer was significantly thicker in the atopic group compared with the group of nonatopic asthmatics. In the atopic group, there was a significant negative correlation between epithelial integrity (defined as the relative length of intact epithelium) and the eosinophil count and also between the number of CD25-positive cells and epithelial integrity. The number of mast cells correlated positively with the thickness of tenascin- and laminin-positive layers. In conclusion, we provide evidence of different patterns of involvement of inflammatory cells in atopic and nonatopic patients with asthma. There were also structural differences in the bronchial mucous membrane between atopic asthma and nonatopic asthma. This suggests that there are differences in the extent of the immunopathologic response of these clinically distinct forms of asthma.
authors: Section of Human Anatomy, Department of Medical Cell Biology, University of Uppsala, Sweden. kawa.amin@genpat.uu.se
authors: K
authors: K
authors: Amin
authors: D
authors: D
authors: Lúdvíksdóttir
authors: C
authors: C
authors: Janson
authors: O
authors: O
authors: Nettelbladt
authors: E
authors: E
authors: Björnsson
authors: G M
authors: GM
authors: Roomans
authors: G
authors: G
authors: Boman
authors: L
authors: L
authors: Sevéus
authors: P
authors: P
authors: Venge
mesh_terms: D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D001706:Biopsy; D001980:Bronchi / Q000378:metabolism / Q000473:pathology*; D016535:Bronchial Hyperreactivity / Q000378:metabolism / Q000473:pathology*; D001991:Bronchitis / Q000378:metabolism / Q000473:pathology*; D016207:Cytokines / Q000378:metabolism; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000378:metabolism / Q000473:pathology*; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D018709:Statistics, Nonparametric; D011795:Surveys and Questionnaires
chemical_list: D016207:Cytokines