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Volume 271, Number 41, Issue of October 11, 1996 pp. 25400-25405
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

Interleukin-8 (IL-8), Melanoma Growth-stimulatory Activity, and Neutrophil-activating Peptide Selectively Mediate Priming of the Neutrophil NADPH Oxidase through the Type A or Type B IL-8 Receptor

(Received for publication, May 13, 1996, and in revised form, July 11, 1996)

Simon P. Green Dagger , Anan Chuntharapai and John T. Curnutte Dagger

From the Departments of Dagger  Immunology and  Bio-analytical Technology, Genentech, Inc., South San Francisco, California 94080

The capacity of neutrophils to generate superoxide (Obardot 2) can be enhanced by prior exposure to ``priming'' agents such as interleukin-8 (IL-8), melanoma growth-stimulatory activity (MGSA), and neutrophil-activating peptide (ENA-78). The biological effects of these chemokines are mediated by at least two distinct receptors: type A (IL-8-RA) and type B (IL-8-RB). Using neutralizing monoclonal antibodies to IL-8-RA and IL-8-RB, we have investigated the contribution each receptor makes to the priming response. Preincubation with IL-8, MGSA, or ENA-78 enhanced the ability of neutrophils to generate Obardot 2 following stimulation with the bacterial peptide formyl-Met-Leu-Phe. The priming effect of IL-8 was eliminated by an anti-IL-8 monoclonal antibody (mAb) that is known to bind IL-8 with high affinity and prevent receptor occupancy. Incubation of neutrophils with a neutralizing mAb specific for IL-8-RA blocked IL-8-induced priming but had no effect on priming by MGSA or ENA-78. In contrast, treatment with a neutralizing mAb specific for IL-8-RB failed to inhibit the priming effect of IL-8 but blocked both MGSA and ENA-78-induced priming. These observations indicate that the priming effect of IL-8 on the neutrophil respiratory burst is predominantly mediated via IL-8-RA, whereas priming by MGSA and ENA-78 is mediated by IL-8-RB.


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