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Interleukin-8 induces the accumulation of B-cell chronic lymphocytic
leukemia cells by prolonging survival in an autocrine fashion
P Francia di Celle, S Mariani, L Riera, A Stacchini, G Reato and R Foa
Dipartimento di Scienze Biomediche e Oncologia Umana, University of Torino,
Italy.
Several cytokines have been suggested to play a regulatory action on the
neoplastic clone of patients with B-cell chronic lymphocytic leukemia
(B-CLL) by interfering in the differentiation, proliferation, or
death/survival pathways. Interleukin-8 (IL-8) is a chemoattractant protein
constitutively expressed at the mRNA level and released by B- CLL cells. In
view of the presence of the IL-8 receptor mRNA and of specific IL-8
binding, confirmed also by Scatchard analysis using 125I- IL-8, the study
was extended to evaluate the possible regulatory role of this cytokine on
B-CLL cells. IL-8 failed to show any in vitro proliferative effect on
leukemic B-CLL cells. By contrast, the propidium iodide (PI) staining of
the DNA content showed that IL-8 could prolong the survival of resting
B-CLL cells in 11 of 16 cases studied. In the remaining 5 cases, 90.6% +/-
4.39% SD of the cells after culture remained viable and IL-8 could exert a
significant death protection action after pretreatment with 10(-4) mol/L
hydrocortisone, which reduced the percentage of viable B-CLL cells. The
dose range of IL-8 capable of inducing the prolonging survival effect is
comparable with the levels of IL-8 released constitutively by B-CLL cells,
indicating that the death protection action is exerted at physiologic
doses. The in vitro rescue from death induced by IL-8 is reflected by an
increased expression of bcl-2 mRNA in B-CLL cases incubated in the presence
of IL-8. These findings were further confirmed at the protein level,
because in B-CLL cells that displayed a bimodal bcl-2 intracytoplasmatic
protein expression IL-8 was capable of upmodulating the bcl-2high
expression peak. The potential autocrine regulatory action exerted by IL-8
is supported by the evidence that exogenous IL-8 can upregulate IL-8 mRNA
in B-CLL cells. These results, together with the demonstration that
antibody-mediated neutralization of endogenous IL-8 could induce a
significant in vitro reduction in the number of living cells, further
support the hypothesis that, in B-CLL, the physiologic doses of IL-8
released constitutively by the leukemic clone may play an autocrine role in
the process of cell accumulation characteristic of this disease.
Volume 87,
Issue 10,
pp. 4382-4389,
05/15/1996
Copyright © 1996 by The American Society of Hematology
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