INVESTIGADORES
CASTRO Marisa Silvia
congresos y reuniones científicas
Título:
E. faecalis: resistencia a la fagocitosis, capacidad inflamatoria y patogenicidad. E. faecalis: phagocytosis resistance, inflammatory capacity and pathogenicity
Autor/es:
SPARO MD; CASTRO MS; MOLINA MA; CECI MA; RANNO G; ANDRÉS MC; HERNÁNDEZ C; SQUIQUERA L; MANGHI MA
Lugar:
Pucón, Chile
Reunión:
Congreso; XVIII Congreso Latinoamericano de Microbiología; 2006
Institución organizadora:
Asociación Latinoamericana de Microbiología
Resumen:
Enterococci are the causative agents of severe infections in immunocompromised hosts. Capsular polysaccharides and opsonising antibodies are considered important factors for the virulence. The resistance of the host¢¥s immune system, the lymphoproliferative response and the secretion of IL-12 were assessed for enterococci isolated from peritoneal exudates and which pathogenicity had previously been studied in Balb/c mice. Eleven strains of E. faecalis were analysed in comparison with environmental (4), probiotic (1), pathogenic from ATCC (1) and isolated from hemocultures (4) strains. The opsonophagocytic activity for each strain was evaluated in the presence of neutrophils, normal rabbit serum and complement (Huebner 1999). Splenocyte suspensions from Balb/c mice were employed to evaluate lymphocyte proliferation (3H-tymidine uptake) and IL-12 production (ELISA) employing each strain as stimulus. Opsonisation percentages ranged from 0% to 96%. Both the probiotic and the environmental strains had a mortality percentge ¡Ã 80%. Hemoculture and ATCC strains displayed a mortality ¡Â 8%. Nine out of the 11 strains showed variable degrees of phagocytosis resistance (4-54% mortality). These results were in line with: *the pathogenicity observed in Balb/c mice, **the lymphoproliferative activity (p<0.001) and ***the IL-12 secretion by macrophages (p<0.05). It could be assumed that the opsonophagocytic activity observed correlates with the presence of a bacterial capsule, which favours the persistence of the pathogen in the bloodstream, thus facilitating the contact with IL-12-secreting macrophages, a sine quanon condition for an inflammatory response to be mounted.
