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Clin Immunol Immunopathol. 1996 Sep;80(3 Pt 1):321-4.

Regulation of human alveolar macrophage inflammatory cytokine production by interleukin-10.

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1
Department of Pulmonary and Critical Care Medicine, Cleveland Clinic Foundation, Ohio 44195-5038, USA.

Abstract

Alveolar macrophages are the primary source of inflammatory cytokine production in the lung. Both site-specific and differentiation-specific factors play a role in cytokine production, and regulation of this activity in alveolar macrophages is distinctly different from that of circulating blood monocytes. Interleukin-10 (IL-10) inhibits the production of inflammatory cytokines [tumor necrosis factor (TNF)-alpha, interleukin-1 (IL-1), interleukin-6 (IL-6), and interleukin-8 (IL-8)] and enhances production of interleukin-1-receptor antagonist (IL-1ra) from endotoxin-stimulated human monocytes, but the effect of IL-10 on such activity in alveolar macrophages is unknown. This study was undertaken to determine the effect of recombinant IL-10 on endotoxin-stimulated cytokine production by human alveolar macrophages. TNF, IL-1, IL-6, and IL-8 secretions were significantly (P < 0.05) stimulated by endotoxin [lipopolysaccharide (LPS)] and were all significantly (P < 0.05) inhibited (median inhibition = 43%) by IL-10 (10 ng/ml). In contrast, IL-1ra was not stimulated by LPS and basal levels were not affected by IL-10. LPS also did not significantly elevate alveolar macrophage IL-10 secretion (< 100 pg/ml) and basal levels were undetectable (< 15 pg/ml). This potent inhibitory activity of IL-10 on inflammatory cytokine production by human alveolar macrophages suggests that exogenous IL-10 may be useful in treatment of inflammatory lung diseases such as adult respiratory distress syndrome.

PMID:
8811054
DOI:
10.1006/clin.1996.0130
[Indexed for MEDLINE]

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