PRODUCTION OF INTERLEUKIN-13 BY ALVEOLAR MACROPHAGES FROM NORMAL AND FIBROTIC LUNG

Citation
A. Hancock et al., PRODUCTION OF INTERLEUKIN-13 BY ALVEOLAR MACROPHAGES FROM NORMAL AND FIBROTIC LUNG, American journal of respiratory cell and molecular biology, 18(1), 1998, pp. 60-65
Citations number
20
Categorie Soggetti
Cell Biology",Biology,"Respiratory System
ISSN journal
10441549
Volume
18
Issue
1
Year of publication
1998
Pages
60 - 65
Database
ISI
SICI code
1044-1549(1998)18:1<60:POIBAM>2.0.ZU;2-D
Abstract
Human interleukin 13 (IL-13) is a cytokine that has a profound effect on primary immune cells by inducing immunoglobulin production, prolife ration of B cells, and the differentiation of cells of the monocytic l ineage, IL-13 can inhibit the production of inflammatory cytokines by both macrophages and monocytes, Previously, IL-13 expression has been reported only in cells of the T-fell lineage and the mast cell line HM C-1. We now report the presence of IL-13 mRNA and protein in human alv eolar macrophages (AMs) analyzed by the reverse transcription-polymera se chain reaction (RT-PCR and enzyme-linked immunoabsorbent assay (ELI SA), respectively, and IL-13 protein in bronchoalveolar lavage fluid ( BALF) of subjects with pulmonary fibrosis, We have investigated 13 pat ients from 49 to 75 yr of age with forms of pulmonary fibrosis, and ei ght healthy volunteers from 24 to G1 yr of age. Their AMs were obtaine d by bronchoalveolar lavage (BAL) and purified by adherence, The propo rtion of BAL purified AMs expressing IL-13 mRNA was increased In those subjects with fibrotic lung disease, in comparison with those from co ntrol subjects (11 of 13 versus 2 of 8, P < 0.01), IL-13 protein was d etectable in the BALF of 8 of 13 patients with pulmonary fibrosis, but in none of the control subjects, AMs of four, subjects with systemic sclerosis were cultured and IL-13 protein was increased in the culture supernatants when compared to the control subjects, although this did not reach significance. These findings show that IL-13 mRNA is not on ly a product of T cells, but is also expressed in both normal AMs and those from subjects with pulmonary fibrosis, and that at least some of the IL-13 mRNA is translated into protein and secreted in subjects wi th pulmonary fibrosis. We hypothesize hat IL-13 may be expressed by no rmal human AMs as part of the homeostatic control process but its prod uction may be increased in the presence of inflammatory lung disease.