title: Aspergillus conidia activate the complement by the mannan-binding lectin C2 bypass mechanism.
abstract: Innate immunity is the major host defense against invasive aspergillosis. To determine whether the collectin mannan-binding lectin (MBL) is involved in the initial protective immunity through complement activation against opportunistic fungal infections caused by Aspergillus, we performed in vitro studies on 29 different strains of Aspergillus conidia from five different species. Incubation of Aspergillus conidia in human normal serum leads to activation of the alternative pathway, whereas neither the classical nor the lectin pathways through C4 and C2 cleavage are activated. Complement response to conidia was investigated using a MBL-deficient serum and reconstitution experiments were conducted with MBL/MASPs complexes. We found that MBL can directly support C3 activation by a C2 bypass mechanism. Finally, a stronger activation of the alternative pathway was observed for the clinical strains isolated from patients with invasive aspergillosis, compared with the environmental strains.
authors.affiliation: Laboratoire Adaptation et Pathogénie des Micro-organismes, Université Joseph Fourier, Grenoble 1, BP 170, Grenoble, France. Chantal.Dumestre@ujf-grenoble.fr
authors.forename: Chantal
authors.initials: C
authors.lastname: Dumestre-Pérard
authors.forename: Bertrand
authors.initials: B
authors.lastname: Lamy
authors.forename: Delphine
authors.initials: D
authors.lastname: Aldebert
authors.forename: Catherine
authors.initials: C
authors.lastname: Lemaire-Vieille
authors.forename: Renée
authors.initials: R
authors.lastname: Grillot
authors.forename: Jean-Paul
authors.initials: JP
authors.lastname: Brion
authors.forename: Jean
authors.initials: J
authors.lastname: Gagnon
authors.forename: Jean-Yves
authors.initials: JY
authors.lastname: Cesbron
mesh_terms: D001230:Aspergillus / Q000276:immunology*; D037582:Complement Pathway, Mannose-Binding Lectin / Q000502:physiology*; D006801:Humans; D013172:Spores, Fungal / Q000276:immunology*