originating from the same state. Strains did also not cluster according to their sources, i.e fromclinical specimen, veterinary or environmental origin. The high diversity among theAustralian strains suggests that S. aurantiacum may have originated within the Australiancontinent and subsequently dispersed to other regions, a fact revealed by the closephlyogenetic relationships between some of the Australian sequence types and those found inother parts of the world. The MLST data are accessible at mlst.mycologylab.org.
ROLE OF PTX3 IN CYSTIC FIBROSIS-ASSOCIATED INFECTIONSYveline Hamon 1,2 , Christine Person 3 , Jean-Louis Giniès 3 , Jean-PhilippeBouchara 4,5 and Yves Delneste 1,21 Inserm U892, Institut de Biologie en Santé-IRIS, Angers, France2 Université d’Angers, Angers, France3 CF Center, Centre Hospitalier Universitaire, Angers, France4 Groupe d'Etude des Interactions Hôte-Pathogène, UPRES-EA 3142, Université d'Angers,Institut de Biologie en Santé-IRIS, Angers, France5 Laboratoire de Parasitologie-Mycologie, Institut de Biologie en Santé-CHU, CentreHospitalier Universitaire, Angers, FrancePTX3, a soluble innate immunity receptor, binds to selected microbes and facilitates theirclearance by phagocytes. PTX3 selectively binds to Pseudomonas aeruginosa and Aspergillusfumigatus, two microorganisms frequently colonizing the airways of patients with cysticfibrosis (CF), and sometimes causing true respiratory infections. PTX3 -/- mice are sensitive toA. fumigatus infection, highlighting the role of this protein in the protection against thispathogen. We thus hypothesized that PTX3 could be altered in CF patients and that this couldbe responsible, at least in part, to their susceptibility to some opportunistic pathogens.Serum and sputum samples from 30 CF patients (20 adults and 15 children) and 7 patientswith chronic obstructive pulmonary disease (COPD) as the control group were analyzed forPTX3 expression and integrity by ELISA and Western-blotting, respectively. The role ofendogenous or microbial proteases on recombinant human PTX3 was also analyzed.Results showed that PTX3 level was increased in CF and COPD serum, highlighting theirinfectious/inflammatory status, while, in contrast, PTX3 concentration was lower orundetectable in CF sputum than in COPD. Western-blotting showed that PTX3 is degraded insputum samples from most of CF patients, but not in clinical specimens from COPD patients.The degradation of PTX3 was shown to be mediated by serine proteases. More precisely, boththe neutrophil elastase and the alkaline proteinase from A. fumigatus have the ability todegrade in vitro PTX3.This study which shows that PTX3 is degraded in respiratory secretions from CF patients,provide new insights into the pathogenesis of microbial colonization of the airways andrespiratory infections in CF patients, since degradation of PTX3 could be responsible, at leastin part, for the sensitivity of CF patients to some opportunistic infections.