Abstract
Abstract Bubonic plague, caused by the gram-negative bacteria Yersinia pestis, is characterized by pathologically swollen lymph nodes (LNs) or buboes. The mechanism by which these buboes form and the adaptive function they provide for the pathogen, if any, remains unknown. We hypothesize that bubo formation is a strategy for flea-borne Y. pestis to establish a foothold in the host for subsequent systemic infection. Our studies indicate that colonization of the draining lymph node (DLN) from the site of infection occurs through the trafficking of infected dendritic cells and monocytes in temporally distinct waves. This is effected by redundant chemotactic signals, including through the receptors CCR7 and CCR2, as evidenced by the upregulation of multiple chemoattractants in the DLN during Y. pestis infection and the improved survival of infected CCR7KO and CCR2KO mice compared to wild-type.
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