Contributors: Groupe d'Étude des Interactions Hôte-Pathogène (GEIHP); Université d'Angers (UA); Génétique Moléculaire Bactérienne; Institut Pasteur Paris (IP); Equipe avenir; Mécanismes moléculaires de la pathogenèse bactérienne; Institut Pasteur de Lille; Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille; Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur Korea - Institut Pasteur de Corée; Réseau International des Instituts Pasteur (RIIP); Laboratoire des mycobactéries; Centre Pasteur du Cameroun; Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP); Centre de Diagnostic et de Traitement de l'Ulcère de Buruli; Programme National de Lutte contre l'Ulcère de Buruli; Ministère de la Santé Publique; Génétique Moléculaire des Levures; Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut Pasteur Paris (IP)-Centre National de la Recherche Scientifique (CNRS); Bioinformatique Structurale; Institut Pasteur Paris (IP)-Centre National de la Recherche Scientifique (CNRS); Service Commun Animalerie hospitalo-universitaire (SCAHU); Immunophysiologie et Parasitisme Intracellulaire; Recherches en cancérologie; Université de Nantes (UN)-IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM); This study was supported by the Ministry of Health, Cotonou, Benin; Centre Hospitalier Universitaire d'Angers (Promoters); the Fondation Raoul Follereau; the Institut National de la Santé et de la Recherche Médicale (INSERM JA, LM, PB ); and the Institut Pasteur (EY, FT, GM, GR, STC).
نبذة مختصرة : International audience ; BACKGROUND: Buruli ulcer is a severe human skin disease caused by Mycobacterium ulcerans. This disease is primarily diagnosed in West Africa with increasing incidence. Antimycobacterial drug therapy is relatively effective during the preulcerative stage of the disease, but surgical excision of lesions with skin grafting is often the ultimate treatment. The mode of transmission of this Mycobacterium species remains a matter of debate, and relevant interventions to prevent this disease lack (i) the proper understanding of the M. ulcerans life history traits in its natural aquatic ecosystem and (ii) immune signatures that could be correlates of protection. We previously set up a laboratory ecosystem with predatory aquatic insects of the family Naucoridae and laboratory mice and showed that (i) M. ulcerans-carrying aquatic insects can transmit the mycobacterium through bites and (ii) that their salivary glands are the only tissues hosting replicative M. ulcerans. Further investigation in natural settings revealed that 5%-10% of these aquatic insects captured in endemic areas have M. ulcerans-loaded salivary glands. In search of novel epidemiological features we noticed that individuals working close to aquatic environments inhabited by insect predators were less prone to developing Buruli ulcers than their relatives. Thus we set out to investigate whether those individuals might display any immune signatures of exposure to M. ulcerans-free insect predator bites, and whether those could correlate with protection. METHODS AND FINDINGS: We took a two-pronged approach in this study, first investigating whether the insect bites are protective in a mouse model, and subsequently looking for possibly protective immune signatures in humans. We found that, in contrast to control BALB/c mice, BALB/c mice exposed to Naucoris aquatic insect bites or sensitized to Naucoris salivary gland homogenates (SGHs) displayed no lesion at the site of inoculation of M. ulcerans coated with Naucoris SGH components. ...
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