Open AccessBrucella requires a functional Type IV secretion system to elicit innate immune responses in mice
Author(s) -
Roux Christelle M.,
Rolán Hortensia G.,
Santos Renato L.,
Beremand Phillip D.,
Thomas Terry L.,
Adams L. Garry,
Tsolis Renée M.
Publication year - 2007
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2007.00922.x
Subject(s) - biology , brucella , innate immune system , immune system , secretion , microbiology and biotechnology , interferon , wild type , proinflammatory cytokine , immunology , gene , mutant , inflammation , genetics , brucellosis , biochemistry
Summary The virB operon, encoding a Type IV secretion system (T4SS), is essential for intracellular survival and persistent infection by Brucella spp. To better understand the role of the T4SS in evading host defence mechanisms and establishing chronic infection, we compared transcriptional profiles of the host response to infection with wild‐type and virB mutant Brucella strains. Analysis of gene expression profiles in murine splenocytes 3 days after inoculation with wild‐type Brucella strains revealed an inflammatory response, with a prominent upregulation of genes induced by both type I and type II interferons. Real‐time RT‐PCR showed that a group of genes from these pathways were induced by day 3 post infection and declined to baseline levels by day 7. In contrast, neither of the two virB mutant strains elicited a proinflammatory gene expression profile, demonstrating that the T4SS was required to trigger this response. Infection studies using type I interferon receptor knockout mice showed that a lack of type I interferon signalling did not affect Brucella replication during the first 4 weeks of infection. Thus, induction of type I interferons does not appear to be an essential mechanism by which the T4SS promotes persistent infection by Brucella .