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 Blood, 15 January 2005, Vol. 105, No. 2, pp. 464-473.
Prepublished online as a Blood First Edition Paper on September 28, 2004; DOI 10.1182/blood-2003-12-4415.

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CHEMOKINES

IL-8 and its CXCR1 and CXCR2 receptors participate in the control of megakaryocytic proliferation, differentiation, and ploidy in myeloid metaplasia with myelofibrosis

Sharareh Emadi, Denis Clay, Christophe Desterke, Bernadette Guerton, Eliane Maquarre, Agnès Charpentier, Claude Jasmin, and Marie-Caroline Le Bousse-Kerdilès, for the French INSERM Research Network on MMM

From the Institut National de la Santé et de la Recherche Médicale (INSERM), Unit 602, André Lwoff Institute, Paul Brousse Hospital, Villejuif, France; Department of Chemical and Material Engineering (CME), Arizona State University, Tempe AZ; and the Laboratory of Hematology, Saint-Vincent Hospital, Groupe Hospitalier de l'Institut Catholique de Lille, Lille Cedex, France.

Myeloproliferation, myelofibrosis, and neoangiogenesis are the 3 major intrinsic pathophysiologic features of myeloid metaplasia with myelofibrosis (MMM). The myeloproliferation is characterized by an increased number of circulating CD34+ progenitors with the prominent amplification of dystrophic megakaryocytic (MK) cells and myeloid metaplasia in the spleen and liver. The various biologic activities of interleukin 8 (IL-8) in hematopoietic progenitor proliferation and mobilization as well as in neoangiogenesis prompted us to analyze its potential role in MMM. We showed that the level of IL-8 chemokine is significantly increased in the serum of patients and that various hematopoietic cells, including platelets, participate in its production. In vitro inhibition of autocrine IL-8 expressed by CD34+ cells with either a neutralizing or an antisense anti–IL-8 treatment increases the proliferation of MMM CD34+-derived cells and stimulates their MK differentiation. Moreover, addition of neutralizing anti–IL-8 receptor (CXC chemokine receptor 1 [CXCR1] or 2 [CXCR2]) antibodies to MMM CD34+ cells cultured under MK liquid culture conditions increases the proliferation and differentiation of MMM CD41+ MK cells and restores their polyploidization. Our results suggest that IL-8 and its receptors participate in the altered MK growth that features MMM and open new therapeutic prospects for this still incurable disease.


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