Abstract
Yersinia pestis, a Gram-negative bacterium and the etiologic agent of plague, has evolved from Yersinia pseudotuberculosis, a cause of a mild enteric disease. However, the molecular and biological mechanisms of how Y. pseudotuberculosis evolved to such a remarkably virulent pathogen, Y. pestis, are not clear. The ability to initiate a rapid bacterial dissemination is a characteristic hallmark of Y. pestis infection. A distinguishing characteristic between the two Yersinia species is that Y. pseudotuberculosis strains possess an O-antigen of lipopolysaccharide (LPS) while Y. pestis has lost the O-antigen during evolution and therefore exposes its core LPS. In this study, we showed that Y. pestis utilizes its core LPS to interact with SIGNR1 (CD209b), a C-type lectin receptor on antigen presenting cells (APCs), leading to bacterial dissemination to lymph nodes, spleen and liver, and the initiation of a systemic infection. We therefore propose that the loss of O-antigen represents a critical step in the evolution of Y. pseudotuberculosis into Y. pestis in terms of hijacking APCs, promoting bacterial dissemination and causing the plague.
Highlights
Yersinia pestis is the bacterium that causes bubonic, septicemic, and pneumonic forms of plague and that was the cause of the Black Death in Europe during the middle ages
We have shown that human DC-specific intercellular adhesion molecule-grabbing nonintegrin, a C-type lectin receptor on antigen presenting cells (APCs) such as macrophages and dendritic cells (DCs), is a receptor for the core LPS of several Gram-negative bacteria, including E. coli, Haemophilus ducreyi, Neisseria gonorrhoeae, Yersinia spp., and Salmonella typhimurium, promoting bacterial adherence and phagocytosis [22,23,24,25,26,27]
Y. pseudotuberculosis strains possess an O-antigen, the production of which was lost by Y. pestis during evolution
Summary
Yersinia pestis is the bacterium that causes bubonic, septicemic, and pneumonic forms of plague and that was the cause of the Black Death in Europe during the middle ages. Recent studies have proved that all three suspected plague pandemics (the Justinian, the Black Death and the third pandemic) were caused by this bacterium [1,2,3,4,5,6]. The apparent question is how did Y. pseudotuberculosis evolve into such a virulent, dangerous and remarkably different pathogen, Y. pestis? A distinguishing difference between these pathogens is that Y. pseudotuberculosis contains an O-antigen of lipopolysaccharide (LPS), which was lost by Y. pestis during its evolution [13,14,15] (Figure 1B). Y. pestis does not contain an O-antigen [14, 15] and the shortened LPS is referred to as lipooligosaccharide (LOS). Why would Y. pseudotuberculosis sacrifice the production of O-Ag, one of its key virulence factors, during the evolution to Y. pestis?
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