The TolC homologue of Brucella suis is involved in resistance to antimicrobial compounds and virulence.

DIANA POSADAS; FERNANDO MARTIN; M J SABIO GARCIA; JUAN M SPERA; M VICTORIA DELPINO; PABLO C BALDI; ELEONORA CAMPOS; SILVIO CRAVERO; ANGELES ZORREGUIETA

INFECTION AND IMMUNITY

AMER SOC MICROBIOLOGY

Año: 2006 p. 379 - 389

0019-9567

Abstract Brucella spp., like other pathogens, must cope with the environment of diverse host niches during the infection process. In doing this, pathogens evolved different type of transport systems to help them survive and disseminate within the host. Members of the TolC family have been shown to be involved in the export of chemically diverse molecules ranging from large protein toxins to small toxic compounds. The role of proteins from the TolC family in Brucella and other á-2 proteobacteria has been little explored. The gene encoding the unique member of the TolC family from Brucella suis (BepC) was cloned and expressed in an E. coli mutant disrupted in the gene encoding TolC that has the peculiarity of being involved in diverse transport functions. BepC fully complemented the resistance to drugs such as chloramphenicol and acriflavine but was incapable to restore hemolysin secretion in the tolC mutant of E. coli. An insertional mutation in the bepC gene strongly affected the resistance phenotype of B. suis to bile salts and toxic chemicals like ethidium bromide and rhodamine and significantly decreased the resistance to antibiotics such as erythromycin, ampicillin, tetracycline and norfloxacin. Moreover, B. suis bepC mutant was attenuated in the mice model of infection. Taken together, these results suggest that BepC-dependent efflux processes of toxic compounds contribute to B. suis survival inside the host.