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
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.