Abstract
Yersinia pestis (Y. Pestis) is an infamous pathogen causing plague pandemics throughout history and is a selected agent of bioterrorism threatening public health. Y. pestis was first isolated by Alexandre Yersin in 1894 in Hong Kong and in the following years from all continents. Plague is enzootic in different rodents and their fleas in Africa, North and South America, and Asia, including the Middle/Far East and ex-USSR countries. Comprehending the multifaceted interaction between Y. pestis and the host immune system will enable us to design more effective vaccines. Innate immune response and both components (humoral and cellular) of adaptive immune response contribute to host defense against Y. pestis infection, but the bacterium possesses different mechanisms to counteract the immune response. The review aims to analyze the role of immune response versus Yersinia pestis infection and to highlight the various stratagems adopted by Y. pestis to escape the immunological defenses.
Highlights
Yersinia pestis was first isolated by AlexandreYersin in 1894 in Hong Kong [1] and the role of fleas in the transmission of plague was subsequently identified [2]
Y. pestis was first isolated by Alexandre Yersin in 1894 in Hong Kong and in the years to follow from all continents
The aims of this review are to analyze the role of immune response versus Yersinia pestis infection and to highlight the various stratagems adopted by Y. pestis to escape the immunological defenses
Summary
Yersin in 1894 in Hong Kong [1] and the role of fleas in the transmission of plague was subsequently identified [2]. The temperature differences from the gut flea (26°C) to the human host (37°C) favor the synthesis of a tetra-acylated form of LPS, that unlike the typical hexa-acylated LPS, it is not able to induce the TLR4mediated production of pro-inflammatory cytokines (IL-1, IL-6, TNF-α, IL-8) [22] In this way, Y. pestis may efficiently block macrophages’ activation and secretion of cytokines, which in turn prevents further activation of dendritic cells, essential for the induction of adaptive immune response [22]. The plague bacilli are able to reduce the host adaptive immune response influencing the cytokine/chemokine induction (discussed in section 1 and in Figure 1) as well as acting directly by the Yops action on the immune cells implicated in the specific immune responses In this way, the inactivation of T cells leading to a reduction of the IFN-γ and TNF-α secretion inhibits the innate responses (Figure 2). The T3SS protein YopH has been previously demonstrated to be able to inhibit the adaptive immune response in vitro [54]
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