Interaction between Yersinia pestis and the Host Immune System

The mammalian immune system comprises multiple physical, chemical, and cellular components that are traditionally classified as innate and adaptive immunity. The innate immune response is the first line of host defense against pathogens, depending on barrier structures, phagocytic cells (neutrophils, macrophages, and dendritic cells [DCs]), natural killer (NK) cells, and molecules such as complement proteins, cytokines, and antimicrobial peptides. Once the bacterium infects the host, the innate immunity provides immediate protection. After 4 to 5 days, the T-cell- and B-cell-mediated adaptive immune response begins to provide organism-specific protection and has a long-lasting immunological memory. In most cases, the bacterium will be eliminated from the host by the synergistic effect of both innate and adaptive immunity. Yersinia pestis, a gram-negative bacterium and plague pathogen, is classified as a category A agent of bioterrorism (18, 19). It gains its notoriety from causing three massive pandemics in history that killed hundreds of millions of people (66). If not treated with proper antimicrobial drugs, the bacteria rapidly escape from containment in the lymph node, spread systemically through the blood, and cause fatal sepsis (66). One of its forms, pneumonic plague, is difficult to treat because of the speed of the disease’s progress (a typical incubation period is 1 to 3 days), and by the time individuals are symptomatic, they are often close to death. To survive inside of the host and maintain a persistent infection, Y. pestis uses a variety of mechanisms to evade or overcome the host immune system, especially the innate immune system. Since the interaction of Y. pestis and host immune system is such a large area of research that it is difficult to cover all aspects in full detail, this review will focus on the following subtopics.