INVESTIGADORES
BIGI Fabiana
artículos
Título:
Knockout mutation of p27?p55 operon severely reduces replication of Mycobacterium bovis in a macrophagic cell line and survival in a mouse model of infection
Autor/es:
MARÍA VERÓNICA BIANCO; FEDERICO CARLOS BLANCO; MARINA ANDREA FORRELLAD; DIANA AGUILAR; CAMPOS ELEONORA; LAURA INÉS KLEPP; ROGELIO HERNÁNDEZ-PANDO; ANGEL ADRIAN CATALDI; FABIANA BIGI
Revista:
Virulence
Editorial:
Landes Bioscience
Referencias:
Año: 2011 vol. 2 p. 233 - 237
ISSN:
2150-5594
Resumen:
Integrity of p27-p55 operon has been demonstrated to be crucial for replication of Mycobacterium tuberculosis, the main agent of human tuberculosis, in the mouse model of infection. However, the individual contribution of each gene of the operon for the virulence of pathogenic Mycobacterium still remains unclear. The operon is formed by two genes, p27 and p55. p27 gene encodes a lipoprotein that binds triacylated glycolipids and modulates the host immune responses by inhibiting the MHC-II Ag processing. Besides, p55 encodes an efflux pump that, together with P27, is involved in resistance to drugs. In this study, we evaluated the individual contribution of P27 and P55 to the virulence of Mycobacterium bovis, the etiological agent for bovine tuberculosis. Knock out mutation of p27-p55 operon in M. bovis severely decreased the virulence of the bacteria when assessed in a progressive model of pulmonary tuberculosis in Balb/c mice. In addition, the mutant strain showed poor replication in a murine macrophagic cell line. Virulence and intracellular replication were only restored when the mutant strain was complemented with a copy of the whole operon. The reintroduction of p55 into the mutant strain partially restored the virulence of the bacteria while low complementation was achieved with p27 individual gene.