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Dermal Neutrophil, Macrophage and Dendritic Cell Responses to Transmitted by Fleas

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Flea-borne transmission is central to the natural history of the plague bacillus Yersinia pestis, and infection within the context of flea feeding may affect the pathogenesis of bubonic plague. We analyzed the mammalian host response to Y. pestis in the skin immediately after transmission by its natural vector, the rat flea Xenopsylla cheopis, to observe differences relative to the response to needle-inoculated bacteria. Our results show that uninfected flea bites induce minimal inflammation, but flea-transmitted Y. pestis cause the recruitment of neutrophils roughly in proportion to the number of bacteria deposited in the skin. We observed interactions of flea-transmitted bacteria with macrophages, a cell type much more permissive than neutrophils for survival and growth of Y. pestis. We found that dendritic cells, important sentinel antigen presenting cells, were recruited to, but had minimal interaction with, flea-transmitted bacteria. Additionally, we found that Y. pestis could disseminate from the flea bite site to the draining lymph node and spleen as early as 1 h after flea feeding, significantly earlier than has been previously reported. This study reveals important differences between needle-inoculated and flea-transmitted Y. pestis in the immediate host response to infection and improves our understanding of the early host-bacterium interactions in plague pathogenesis.

Vyšlo v časopise: Dermal Neutrophil, Macrophage and Dendritic Cell Responses to Transmitted by Fleas. PLoS Pathog 11(3): e32767. doi:10.1371/journal.ppat.1004734
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004734

Souhrn

Flea-borne transmission is central to the natural history of the plague bacillus Yersinia pestis, and infection within the context of flea feeding may affect the pathogenesis of bubonic plague. We analyzed the mammalian host response to Y. pestis in the skin immediately after transmission by its natural vector, the rat flea Xenopsylla cheopis, to observe differences relative to the response to needle-inoculated bacteria. Our results show that uninfected flea bites induce minimal inflammation, but flea-transmitted Y. pestis cause the recruitment of neutrophils roughly in proportion to the number of bacteria deposited in the skin. We observed interactions of flea-transmitted bacteria with macrophages, a cell type much more permissive than neutrophils for survival and growth of Y. pestis. We found that dendritic cells, important sentinel antigen presenting cells, were recruited to, but had minimal interaction with, flea-transmitted bacteria. Additionally, we found that Y. pestis could disseminate from the flea bite site to the draining lymph node and spleen as early as 1 h after flea feeding, significantly earlier than has been previously reported. This study reveals important differences between needle-inoculated and flea-transmitted Y. pestis in the immediate host response to infection and improves our understanding of the early host-bacterium interactions in plague pathogenesis.

Zdroje

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