Abstract
Brucella spp. are facultative intracellular pathogens that have the ability to survive and multiply in professional and non-professional phagocytes, and cause abortion in domestic animals and undulant fever in humans. Several species are recognized within the genus Brucella and this classification is mainly based on the difference in pathogenicity and in host preference. Brucella strains may occur as either smooth or rough, expressing smooth LPS (S-LPS) or rough LPS (R-LPS) as major surface antigen. This bacterium possesses an unconventional non-endotoxic lipopolysaccharide that confers resistance to anti-microbial attacks and modulates the host immune response. The strains that are pathogenic for humans (B. abortus, B. suis, B. melitensis) carry a smooth LPS involved in the virulence of these bacteria. The LPS O-chain protects the bacteria from cellular cationic peptides, oxygen metabolites and complement-mediated lysis and it is a key molecule for Brucella survival and replication in the host. Here, we review i) Brucella LPS structure; ii) Brucella genome, iii) genes involved in LPS biosynthesis; iv) the interaction between LPS and innate immunity.
Highlights
Brucellae are Gram-negative cocccobacilli, facultative intracellular bacterial pathogens of both humans and animals
The bacteria penetrate the mucosa of the nasal, oral, or pharyngeal cavities and are phagocytized by host macrophages, where survival and replication occurs
Six species are recognized within the genus Brucella: B. abortus, B. melitensis, B. suis, B. ovis, B. canis, and B. neotomae
Summary
Brucellae are Gram-negative cocccobacilli, facultative intracellular bacterial pathogens of both humans and animals. A mutant strain was characterized by a truncated rough LPS and DNA sequence analysis of this mutant revealed a transposon interruption in the gene encoding phosphomannomutase (pmm or manB), suggesting that this activity may be required for the synthesis of a full-length core polysaccharide in addition to O-antigen. This gene is responsible for the interconversion of mannose-6-phosphate and mannose-1-phosphate. The consequence of TLR9 engagement is that Th1-like responses such as IFN-g production takes place in wild-type but not TLR9 KO mice
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