The infective phenotype favors B. pertussis survival in immune cells.

LAMBERTI, YANINA; GORGOJO, JUAN ; PEREZ VIDAKOVICS, M.LAURA; RODRIGUEZ, M.EUGENIA.

Mar del Plata, Buenos Aires, Argentina.

Congreso; XLIII Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB).; 2007

Bordetella pertussis (Bp), the etiologic agent of Pertussis, expresses adhesins and toxins like Filamentous Hemagglutinin (FHA) or Adenylate cyclase (AC) that play a role in pathogenesis. The expression of these proteins varies in response to environmental signals. Current evidence indicates that the infective phenotype of Bp might express FHA but not AC or other toxins are present. The innate interaction of the bacteria with immune cells is not yet clear. We found that CR3 (via FHA) and cholesterol rich domains are critical for Bp binding to immune cells and involved in bacterial delivery to non-lysosomal compartments. Several studies indicate that AC has a role in Bp survival in immune cells. In this study we investigated the interaction of Bp wild type (wt) and AC deficient mutant with human monocytes (U937) by flow cytometry and fluorescence microscopy. We found that the lack of AC expression determined a higher attachment and internalization of Bp. Confocal studies indicated that in contrast to IgG-opsonized Bp, wt failed to fuse with lysosomas. Interestingly, the lack of AC increased the number of Bp colocalizing with lysosmes but survival studies showed an increased number of alive bacteria inside the cells probably due to the higher rate of internalization. These results support the hypothesis that virulence modulation contributes to Bp survival in the infected hosts