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Signal pathway regulation of interleukin-8-induced actin polymerization in
neutrophils
RL Sham, PD Phatak, TP Ihne, CN Abboud and CH Packman
University of Rochester School of Medicine and Dentistry, NY.
Interleukin-8 (IL-8), a recently described peptide cytokine, is a
neutrophil chemoattractant and activator that exerts effects similar to
fMLP, yet their receptors and their roles in pathophysiology differ. The
effect of IL-8 on the neutrophil cytoskeleton has not been well studied;
therefore, we compared and contrasted the effects of IL-8 and fMLP on
neutrophil actin conformation and on the signal pathway regulation of actin
responses. IL-8 caused a rapid, dose-dependent increase in neutrophil
F-actin content within 30 seconds. The maximum increase was twofold. These
changes were accompanied by the development of F-actin-rich pseudopods, as
noted with fluorescence microscopy and scanning electron microscopy.
Selected biochemical inhibitors were used to study the regulation of the
IL-8-induced actin changes. Incubation of neutrophils with 2 micrograms/mL
pertussis toxin resulted in a 67% inhibition of the IL-8-induced F-actin
increase. The protein kinase C (PKC) inhibitors, staurosporine and H7, did
not inhibit the increase in F-actin caused by IL-8. IL-8 caused a rapid
increase in neutrophil intracellular calcium that could be completely
inhibited by the chelating agent
1,2-bis(o-aminophenoxy)ethane-N,N-N',N'-tetraacetic acid (BAPTA). However,
BAPTA-treated neutrophils retained the ability to increase F-actin in
response to IL-8. Similar results were seen with fMLP, indicating that,
similar to fMLP, the IL-8-induced actin response is mediated through
pertussis-toxin-sensitive G-proteins but is neither dependent on PKC nor
increases in cytosolic calcium. Thus, although IL- 8 and fMLP exert their
effects on neutrophils through different receptors, the signal transduction
pathways used and the effects on actin conformation and pseudopod formation
are similar.
Volume 82,
Issue 8,
pp. 2546-2551,
10/15/1993
Copyright © 1993 by The American Society of Hematology
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