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Oxidative burst in lipopolysaccharide-activated human alveolar macrophages is inhibited by interleukin-9

¹ Experimental Medicine Unit, ² Ludwig Institute for Cancer Research (Brussels branch), Christian de Duve Institute of Cellular Pathology, and ³ Laboratory of Haematology, Université de Louvain, Brussels, Belgium

CORRESPONDENCE: C. Pilette, Unité de Médecine expérimentale, Avenue Hippocrate 74 BP 7430, B-1200, Bruxelles, Belgique. Fax: 32 27647430. E-mail: charles.pilette@mexp.ucl.ac.be

Keywords: cytokine, deactivation, interleukin, lipopolysaccharide, lung, macrophage

Received: January 23, 2002
Accepted June 10, 2002

C. Pilette is currently Aspirant of the Fonds National de la Recherche Scientifique (Belgium, Grant no. 3.4590.99), and Y. Ouadrhiri is supported by the Fondation Lancardis (Switzerland).

Interleukin (IL)-9 is known to regulate many cell types involved in T-helper type 2 responses classically associated with asthma, including B- and T-lymphocytes, mast cells, eosinophils and epithelial cells. In contrast, target cells mediating the effects of IL-9 in the lower respiratory tract remain to be identified. Therefore, the authors evaluated the activity of IL-9 on human alveolar macrophages (AM) from healthy volunteers.

AM preincubated with IL-9 before lipopolysaccharide (LPS) stimulation exhibited a decreased oxidative burst, as previously shown with IL-4. The inhibitory effect of IL-9 was abolished by anti-hIL-9R monoclonal antibody, and presence of IL-9 receptors on AM was demonstrated by immunofluorescence. Both IL-4 and IL-9 failed to modulate tumour necrosis factor-, IL-8 and IL-10 release by LPS-stimulated AM. However, several observations suggested that IL-9 and IL-4 act through different mechanisms: 1) interferon- antagonised the IL-4- but not the IL-9-mediated inhibition of AM oxidative burst; 2) expression of CD14 was downregulated by IL-4 but not by IL-9 and 3) production of tumour growth factor-ß by activated AM was potentiated by IL-9 and not by IL-4, and was required for the IL-9-mediated inhibition of AM oxidative burst.

These observations provide additional information concerning the activity of interleukin-9 in the lung, related to inflammatory or fibrosing lung processes.

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