Abstract
In the past several years neutrophil attractant/activation protein-1 (interleukin-8, NAP- 1/IL-8) had been characterized as potent neutrophil and lymphocyte agonist (1) produced by a wide variety of cells in different tissues upon stimulation either by major inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor (TNF) or by microorganisms and their products (1,2). When injected into humans and experimental animals NAP-1/IL-8 was shown to induce, depending on the route of injection, either leukocytosis and neutrophil accumulation in the lungs (3) or leukocyte emigration into the peripheral injection sites (4-7). In addition, it was linked by a multitude of studies to the pathogenesis of human and experimental inflammatory diseases including adult respiratory distress syndrome (3), chronic inflammatory bowel disease (8), rheumatoid arthritis (9,10), gout (11), asbestosis (12), empyema (13), etc. As a result, generally accepted view emerged that the in vivo production of NAP-I/IL-8 is always associated with pathological conditions, mainly, various forms of inflammation and malignancy. In sharp contrast to this view, here we provide evidence that NAP-1/IL-8 is produced and secreted in substantial quantities by several exocrine glands under either physiological, special physiological or “physiological stress” conditions in normal healthy humans. The glands secreting NAP-1/1L-8 include eccrine sweat glands, mammary glands, lacrimal glands, major salivary glands and minor salivary glands of the oral mucosa. We speculate on the possible role this chemokine plays as a homeostatic mediator responsible for the mucosal host defenses and leukocyte extravasation into the normal tissues.
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Rot, A., Jones, A.P., Webb, L.M.C. (1993). Some Aspects of NAP-1/IL-8 Pathophysiology II: Chemokine Secretion by Exocrine Glands. In: Lindley, I.J.D., Westwick, J., Kunkel, S. (eds) The Chemokines. Advances in Experimental Medicine and Biology, vol 351. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2952-1_9
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DOI: https://doi.org/10.1007/978-1-4615-2952-1_9
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