INVESTIGADORES
GIAMBARTOLOMEI Guillermo Hernan
artículos
Título:
Brucella abortus induces collagen deposition and MMP-9 down-modulation in hepatic stellate cells via TGFâ-1 production
Autor/es:
ARRIOLA BENITEZ P. C., SCIAN R., COMERCI D. J., REY SERANTES D., VANZULLI S., FOSSATI C. A., GIAMBARTOLOMEI G. H., DELPINO M. V.
Revista:
AMERICAN JOURNAL OF PATHOLOGY
Editorial:
AMER SOC INVESTIGATIVE PATHOLOGY, INC
Referencias:
Lugar: Bethesda ; Año: 2013 vol. 183 p. 1918 - 1927
ISSN:
0002-9440
Resumen:
In patients with active brucellosis, the liver is frequently affected by histopathologic lesions, such as
granulomas, inflammatory infiltrations, and parenchymal necrosis. Herein, we examine some potential
mechanisms of liver damage in brucellosis. We demonstrate that Brucella abortus infection inhibits matrix
metalloproteinase-9 (MMP-9) secretion and induces collagen deposition and tissue inhibitor of matrix
metalloproteinase-1 secretion induced by hepatic stellate cells (LX-2). These phenomena depend on
transforming growth factor-b1 induction. In contrast, supernatants from B. abortuseinfected hepatocytes
and monocytes induce MMP-9 secretion and inhibit collagen deposition in hepatic stellate cells. Yet,
if LX-2 cells are infected with B. abortus, the capacity of supernatants from B. abortuseinfected hepatocytes
and monocytes to induce MMP-9 secretion and inhibit collagen deposition is abrogated. These
results indicate that depending on the balance between interacting cells and cytokines of the surrounding
milieu, the response of LX-2 cells could be turned into an inflammatory or fibrogenic phenotype. Livers
from mice infected with B. abortus displayed a fibrogenic phenotype with patches of collagen deposition
and transforming growth factor-b1 induction. This study provides potential mechanisms of liver immune
response induced by B. abortuseinfected hepatic stellate cells. In addition, these results demonstrate
that the cross talk of these cells with hepatocytes and macrophages implements a series of interactions
that may contribute to explaining some of mechanisms of liver damage observed in human brucellosis.