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* Centre National de la Recherche Scientifique FRE2933, Laboratoire de Neuroimmunologie des Annélides and
Institut National de la Santé et de la Recherche Médicale, Unité 800, Laboratoire de Physiologie Cellulaire, Université de Lille 1, Villeneuve d’Ascq, France;
Department of Zoophysiology, Zoological Institute, University of Kiel, Kiel, Germany; and
Section of Cell and Developmental Biology, Division of Biological Sciences, University of California, La Jolla, CA 92093
Following trauma, the CNS of the medicinal leech, unlike the mammalian CNS, has a strong capacity to regenerate neurites and synaptic connections that restore normal function. In this study, we show that this regenerative process is enhanced by a controlled bacterial infection, suggesting that induction of regeneration of normal CNS function may depend critically upon the coinitiation of an immune response. We explore the interaction between the activation of a neuroimmune response and the process of regeneration by assaying the potential roles of two newly characterized antimicrobial peptides. Our data provide evidence that microbial components differentially induce the transcription, by microglial cells, of both antimicrobial peptide genes, the products of which accumulate rapidly at sites in the CNS undergoing regeneration following axotomy. Using a preparation of leech CNS depleted of microglial cells, we also demonstrate the production of antimicrobial peptides by neurons. Interestingly, in addition to exerting antibacterial properties, both peptides act as promoters of the regenerative process of axotomized leech CNS. These data are the first to report the neuronal synthesis of antimicrobial peptides and their participation in the immune response and the regeneration of the CNS. Thus, the leech CNS appears as an excellent model for studying the implication of immune molecules in neural repair.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by the Centre National de la Recherche Scientifique, the Ministère de l’Enseignement, de la Recherche et des Technologies, the National Institute of Health-Fogarty Program, the Genoscope, and the Deutsche Forschungsgemeinschaft (SFB 617, TP 18).
2 The nucleotide sequences reported in this article have been submitted to the GenBankTM/European Bioinformatics Institute Data Bank with accession numbers EU156754, EU156755, EU156756, and EU164975.
3 Address correspondence and reprint requests to Dr. Aurélie Tasiemski, Laboratoire de Neuroimmunologie des Annélides, Centre National de la Recherche Scientifique FRE2933, Groupe "Signaux de Danger, Voies de Signalisation et Effecteurs" Université des Sciences et Technologies de Lille1, 59655 Villeneuve d’Ascq, Cedex, France. E-mail address: aurelie.tasiemski{at}univ-lille1.fr
4 Abbreviations used in this paper: ACN, acetonitrile; RP, reversed phase; DIA, dot-immunoblotting assay; EST, expressed sequence tag; RT, reverse transcriptase; Ct, cycle threshold; Ct, cycle threshold; NGS, normal goat serum; ISH, in situ hybridization.
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