RELATIVE RELEASE OF INTERLEUKIN-1-BETA AND INTERLEUKIN-1 RECEPTOR ANTAGONIST BY ALVEOLAR MACROPHAGES - A STUDY IN ASBESTOS-INDUCED LUNG-DISEASE, SARCOIDOSIS, AND IDIOPATHIC PULMONARY FIBROSIS
Jn. Kline et al., RELATIVE RELEASE OF INTERLEUKIN-1-BETA AND INTERLEUKIN-1 RECEPTOR ANTAGONIST BY ALVEOLAR MACROPHAGES - A STUDY IN ASBESTOS-INDUCED LUNG-DISEASE, SARCOIDOSIS, AND IDIOPATHIC PULMONARY FIBROSIS, Chest, 104(1), 1993, pp. 47-53
We examined the influence of untreated interstitial lung disease (ILD)
on the in vitro release of interleukin-1beta (IL-1beta) and interleuk
in-1 receptor antagonist (IL-1ra) from alveolar macrophages (AM); AM w
ere harvested from normal volunteers, ILD patients, and patients with
asbestos-related pleural disease but no ILD. AM were cultured for 24 h
and assays for IL-1beta and IL-1ra were done using sensitive and spec
ific enzyme-linked immunosorbent assay. A greater amount of IL-1beta w
as detected in AM supernatants from asbestosis, sarcoidosis, and IPF p
atients than in those from normal subjects. The IL-1beta:IL-1ra ratio
(IL-1beta activity index [IL-1AI]) was significantly lower in supernat
ants of normal macrophages compared with macrophage supernatants from
individuals with ILD. The IL-1AI correlated with bronchoalveolar lavag
e cellularity, a marker of disease activity. Current smoking was assoc
iated with lower IL-1beta and IL-1ra release in ILD. The IL-1AI is a c
onvenient method for comparison of IL-1beta activity between patient p
opulations.