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

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Abstract
The relationship between zinc treatment and interleukin-1 α (IL-1α) production by cultured alveolar macrophages (AM) in patients with pulmonary tuberculosis and bacterial pneumonia was investigated. AM (1×106 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 μg/ml and Zn2=5 μg/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-1α in culture supernatants was measured by enzyme-linked immunosorbent assay (ELISA). In the absence of Zn1 or Zn2 Polyinosinic: Polycytidylic acid (Poly I:C 1 μg/ml), Lipopolysaccharide (LPS 100 ng/ml) and Tumour necrosis factor-α (TNF-α 10 ng/ml) significantly increased the production of IL-1α 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-1α (p<0.001) in culture supernatants in the absence of either Poly I:C, LPS or TNF-α in patients but not in healthy group. In contrast, the presence of LPS or TNF-α significantly reduced Zn1 or Zn2-stimulated release of IL-1α from AM in patients and healthy subjects (p<0.01). However, Poly I:C decreased only Zn1-stimulated release of IL-1α. These results suggest that zinc can regulate the production of IL-1α from AM in patients with pulmonary tuberculosis or bacterial pneumonia.