INVESTIGADORES
GIAMBARTOLOMEI Guillermo Hernan
artículos
Título:
The Effector Protein BPE005 from Brucella abortus Induces Collagen Deposition and Matrix Metalloproteinase 9 Downmodulation via Transforming Growth Factor β1 in Hepatic Stellate Cells
Autor/es:
ARRIOLA BENITEZ P. C., REY SERANTES D., HERRMANN C. K., PESCE VIGLIETTI A. I., VANZULLI S., GIAMBARTOLOMEI G. H., COMERCI D. J., DELPINO M. V. 2015
Revista:
INFECTION AND IMMUNITY
Editorial:
AMER SOC MICROBIOLOGY
Referencias:
Lugar: Washington; Año: 2016 vol. 84 p. 598 - 606
ISSN:
0019-9567
Resumen:
The liver is frequently affected in patients with active brucellosis. In the present study, we identified a virulence factor involvedin the modulation of hepatic stellate cell function and consequent fibrosis during Brucella abortus infection. This study assessedthe role of BPE005 protein from B. abortus in the fibrotic phenotype induced on hepatic stellate cells during B. abortus infectionin vitro and in vivo. We demonstrated that the fibrotic phenotype induced by B. abortus on hepatic stellate (LX-2) cells was dependenton BPE005, a protein associated with the type IV secretion system (T4SS) VirB from B. abortus. Our results indicatedthat B. abortus inhibits matrix metalloproteinase 9 (MMP-9) secretion through the activity of the BPE005-secreted protein andinduces concomitant collagen deposition by LX-2 cells. BPE005 is a small protein containing a cyclic nucleotide monophosphatebinding domain (cNMP) that modulates the LX-2 cell phenotype through a mechanism that is dependent on the cyclic AMP(cAMP)/protein kinase A (PKA) signaling pathway. Altogether, these results indicate that B. abortus tilts LX-2 cells to a profibrogenicphenotype employing a functional T4SS and the secreted BPE005 protein through a mechanism that involves the cAMPand PKA signaling pathway.