Ht. Abul et al., INTERLEUKIN-1-ALPHA (IL-1-ALPHA) PRODUCTION BY ALVEOLAR MACROPHAGES IN PATIENTS WITH ACUTE LUNG-DISEASES - THE INFLUENCE OF ZINC SUPPLEMENTATION, Molecular and cellular biochemistry, 146(2), 1995, pp. 139-145
The relationship between zinc treatment and interleukin-1 alpha (IL-1
alpha) production by cultured alveolar macrophages (AM) in patients wi
th pulmonary tuberculosis and bacterial pneumonia was investigated. AM
(1 x 10(6) cells/ml) from 6 patients with pulmonary tuberculosis, 7 p
atients with bacterial pneumonia and 4 healthy volunteers were culture
d with either two different concentrations of zinc chloride (Zn1 = 1 m
u g/ml and Zn2 = 5 mu g/ml) or cell culture media alone (control) for
an initial period of 6 hours and then stimulated with 3 different immu
nomodulator agents and reincubated for a further 24 h. IL-1 alpha in c
ulture supernatants was measured by enzyme-linked immunosorbent assay
(ELISA). In the absence of Zn1 or Zn2 Polyinosinic:Polycytidylic acid
(Poly I:C1 mu g/ml), Lipopolysaccharide (LPS 100 ng/ml) and Tumour nec
rosis factor-alpha (TNF-alpha 10 ng/ml) significantly increased the pr
oduction of IL-1 alpha from AM in both patients and healthy subjects (
p < 0.001) compared to control (media only). Zn1 and Zn2 significantly
increased the production of IL-1 alpha (p < 0.001) in culture superna
tants in the absence of either Poly I:C, LPS or TNF-alpha in patients
but not in healthy group. In contrast, the presence of LPS or TNF-a si
gnificantly reduced Zn1 or Zn2-stimulated release of IL-1 alpha from A
M in patients and healthy subjects (p < 0.01). However, Poly I:C decre
ased only Zn1-stimulated release of IL-1 alpha. These results suggest
that zinc can regulate the production of IL-1 alpha from AM in patient
s with pulmonary tuberculosis or bacterial pneumonia.