title: Pleural cellular reaction to the filarial infection Litomosoides sigmodontis is determined by the moulting process, the worm alteration, and the host strain.
abstract: The filarial nematode Litomosoides sigmodontis model was used to decipher the complex in vivo relationships between filariae, granulomas and leukocytes in the host's pleural cavity. The study was performed from D5 p.i.: to D47 p.i. in resistant C57BL/6 mice, to D74 p.i. in susceptible BALB/c mice, and to D420 p.i. in permissive jirds. We showed that, during the first month, leukocytes only clustered as granulomas around shed cuticles (exuviae) and with eosinophils as the major constituents. In addition, carbohydrates residues became abundant on exuviae only, suggesting a glycan-dependent mechanism of eosinophil attachment. Neutrophils were absent from the pleural cavity of all rodents and from the murine granulomas, but they made up 25% of the granuloma cell population in jirds. After the first month of infection granulomas formed around developed adult worms and morphological evidence suggested that leukocytes preferentially clustered around altered, but still motile, worms. No carbohydrates were detected on these worms and neutrophils were abundant in those granulomas. Finally, a rare third type of granuloma was observed in the resistant mice only; they contained young newly moulted adult worms; typically these granulomas were attached to the lateral lines of the worm via eosinophils; this feature correlated with the persistence of carbohydrate residues on the worms' lateral lines. Neutrophils were always in low proportion in all granulomas from resistant mice, suggesting difference in their adhesive properties in these mice. In vitro neutrophil recruitment in resistant mice was similar to that observed in susceptible mice although they expressed less cell surface CD11b.
authors.affiliation: USM 307, Parasitologie comparée et Modèles expérimentaux, Muséum National d'Histoire Naturelle, 61 rue Buffon, CP52, Paris Cedex 05, France.
authors.forename: Tarik
authors.initials: T
authors.lastname: Attout
authors.forename: Coralie
authors.initials: C
authors.lastname: Martin
authors.forename: Simon A
authors.initials: SA
authors.lastname: Babayan
authors.forename: Wieslaw J
authors.initials: WJ
authors.lastname: Kozek
authors.forename: Chiara
authors.initials: C
authors.lastname: Bazzocchi
authors.forename: François
authors.initials: F
authors.lastname: Oudet
authors.forename: Iain J
authors.initials: IJ
authors.lastname: Gallagher
authors.forename: Sabine
authors.initials: S
authors.lastname: Specht
authors.forename: Odile
authors.initials: O
authors.lastname: Bain
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D004804:Eosinophils / Q000276:immunology; D005260:Female; D005368:Filariasis / Q000276:immunology / Q000469:parasitology / Q000503:physiopathology; D005370:Filarioidea / Q000254:growth & development / Q000472:pathogenicity*; D005849:Gerbillinae / Q000469:parasitology; D006099:Granuloma / Q000276:immunology; D006790:Host-Parasite Interactions; D006801:Humans; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018978:Molting; D009504:Neutrophils / Q000276:immunology; D035422:Pleural Cavity / Q000166:cytology / Q000276:immunology / Q000503:physiopathology; D013045:Species Specificity