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

Pilette, Charles;Ouadrhiri, Y;Van Snick, Jacques;Renauld, Jean-Christophe;Sibille, Yves;et.al.
(2002) The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology — Vol. 20, n° 5, p. 1198-1205 (2002)

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Authors
  • Pilette, CharlesUCLouvain
    Author
  • Ouadrhiri, YUCLouvain
    Author
  • Van Snick, JacquesUCLouvain
    Author
  • Renauld, Jean-Christopheorcid-logoUCLouvain
    Author
  • Staquet, P.UCLouvain
    Author
  • Vaerman, Jean-PierreUCLouvain
    Author
  • Sibille, YvesUCLouvain
    Author
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Abstract
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 alpha 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-alpha, 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-gamma antagonised the IL4- 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-beta by activated AM was potentiated by IL-9 and not by IL4, 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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Pilette, C., Ouadrhiri, Y., Van Snick, J., Renauld, J.-C., Staquet, P., Vaerman, J.-P., & Sibille, Y. (2002). Oxidative burst in lipopolysaccharide-activated human alveolar macrophages is inhibited by interleukin-9. The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology, 20(5), 1198-1205. https://doi.org/10.1183/09031936.02.00005402 (Original work published 2002)