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Retrovirology. 2009; 6: 29.
Published online 2009 March 24. doi: 10.1186/1742-4690-6-29.
PMCID: PMC2667475
Increased neutrophil apoptosis in chronically SIV-infected macaques
Carole Elbim,1 Valérie Monceaux,2 Stéphanie François,3 Bruno Hurtrel,2 Marie-Anne Gougerot-Pocidalo,3 and Jérome Estaquiercorresponding author2,4,5
1Centre de Recherche des Cordeliers, Université Pierre et Marie Curie – Paris 6, UMR S 872, Paris, F-75006 France; Université Paris Descartes, UMR S 872, Paris, F-75006, France
2Institut Pasteur, Unité de Physiopathologie des Infections Lentivirales, Paris, F-75015, France
3AP-HP, Centre Hospitalier Universitaire Xavier Bichat, Service d'Immunologie et d'Hématologie, Paris, F-75018, France
4INSERM, U841, Faculté de Médecine de Créteil, Créteil, F-94010, France
5AP-HP, Hôpital Henri Mondor, Créteil, F-94010, France
corresponding authorCorresponding author.
Carole Elbim: carole.elbim/at/crc.jussieu.fr; Valérie Monceaux: valerie.monceaux/at/pasteur.fr; Stéphanie François: francois/at/inserm.fr; Bruno Hurtrel: bruno.hurtrel/at/pasteur.fr; Marie-Anne Gougerot-Pocidalo: marianne.pocidalo/at/bch.aphp.fr; Jérome Estaquier: estaquier/at/yahoo.fr
Received November 14, 2008; Accepted March 24, 2009.
Abstract
Polymorphonuclear neutrophils (PMN) from chronically HIV-infected individuals have been reported to be more prone to die. However, although non-human primates models have been extensively used for improving our knowledge on T cell immunity, the impact of SIV-infection on PMN, in relationships with disease severity, has never been assessed. In our study, we demonstrate that PMN from Rhesus macaques (RMs) of Chinese origin chronically infected with the virulent strain SIVmac251 display increased susceptibility to undergo apoptosis as compared to PMN from RMs infected with the non-pathogenic SIVΔnef strain. PMN apoptosis was significantly increased in RMs progressing faster to AIDS as compared to non-progressors RMs. Furthermore, the percentage of apoptotic cells correlated with PMN activation state reflected by increased CD11b expression and reactive oxygen species production. Interestingly, whereas inflammatory cytokines IL-8 and IL-1β prevent in vitro PMN death, the levels of those cytokines were low in RMs progressing towards AIDS. Altogether, increased PMN death during SIV infection is a new pathogenic effect associated with AIDS progression, adding to the long list of markers associated with disruption of defense against infection.