High concentrations of beta-chemokines in BAL fluid of patients with diffuse panbronchiolitis

Citation
J. Kadota et al., High concentrations of beta-chemokines in BAL fluid of patients with diffuse panbronchiolitis, CHEST, 120(2), 2001, pp. 602-607
Citations number
17
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CHEST
ISSN journal
00123692 → ACNP
Volume
120
Issue
2
Year of publication
2001
Pages
602 - 607
Database
ISI
SICI code
0012-3692(200108)120:2<602:HCOBIB>2.0.ZU;2-I
Abstract
Background: T cells are important cellular components of bronchial inflamma tion in diffuse panbronchiolitis (DPB). beta -Chemokines such as RANTES (re gulated on activation, normal T-cell expressed and secreted) and macrophage inflammatory peptide (MIP)-1 alpha are closely related to the migration of inflammatory cells into the lung. In this study, we investigate the contri bution of beta -chemokines to the accumulation of T cells in the lungs of p atients with DPB. Patients and methods: We determined the levels of beta -chemokines in BAL f luid (BALF) and the correlation between these levels and T-cell subsets in BALF of 23 patients with DPB and 16 healthy subjects by sandwich enzyme-lin ked immunosorbent assay and flow cytometry. Results: Percentages of CD3+ human leukocyte antigen (HILA)-DR+, CD8+, and CD8+HLA-DR+ cells in BALF of patients were significantly higher than in the control BALF. The absolute number of CD8+HLA-DR+ cells was also higher in RALF of patients than in the control BALF (p < 0.0001). Phenotypic analysis of CD4+ cells in BALF showed a similar percentage of CD4+CD45RA+ cells and CD4+CD29+ cells in patients and normal subjects. The concentrations of RAN TES and MIP-1<alpha> in RALF of patients with DPB were significantly higher than in BALF of normal subjects (p < 0.05). In addition, there was a signi ficant correlation between the absolute number or percentage of CD8+HILA-DR + cells and MIP-1<alpha> concentration in BALF. Conclusions: Our results suggest that the interaction between activated CD8 + T cells and MIP-1 alpha may contribute to the pathogenesis of DPB.