Interleukin-1 alpha (IL-1 alpha) production by alveolar macrophages in patients with acute lung diseases: the influence of zinc supplementation.

Abstract

The relationship between zinc treatment and interleukin-1 alpha (IL-1 alpha) production by cultured alveolar macrophages (AM) in patients with pulmonary tuberculosis and bacterial pneumonia was investigated. AM (1 x 10(6) cells/ml) from 6 patients with pulmonary tuberculosis, 7 patients with bacterial pneumonia and 4 healthy volunteers were cultured with either two different concentrations of zinc chloride (Znl = 1 microgram/ml and Zn2 = 5 micrograms/ml) or cell culture media alone (control) for an initial period of 6 hours and then stimulated with 3 different immunomodulator agents and reincubated for a further 24 h. IL-1 alpha in culture supernatants was measured by enzyme-linked immunosorbent assay (ELISA). In the absence of Znl or Zn2 Polyinosinic:Polycytidylic acid (Poly I:C 1 microgram/ml), Lipopolysaccharide (LPS 100 ng/ml) and Tumour necrosis factor-alpha (TNF-alpha 10 ng/ml) significantly increased the production 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 supernatants 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-alpha significantly reduced Zn1 or Zn2-stimulated release of IL-1 alpha from AM in patients and healthy subjects (p < 0.01). However, Poly I:C decreased only Zn1-stimulated release of IL-1 alpha. These results suggest that zinc can regulate the production of IL-1 alpha from AM in patients with pulmonary tuberculosis or bacterial pneumonia.