English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

We are using a systemic plague model to identify the cells and pathways that are undermined by the virulence protein YopM of the plague bacteriumYersinia pestis . In this study, we pursued previous findings that Gr1+ cells are required to selectively limit growth of ΔyopM Y. pestis and that CD11b+ cells other than polymorphonuclear leukocytes (PMNs) are selectively lost in spleens infected with parentY. pestis . When PMNs were ablated from mice, ΔyopM Y. pestis grew as well as the parent strain in liver but not in spleen, showing that these cells are critical for controlling growth of the mutant in liver but not spleen. In mice lacking expression of the chemokine receptor CCR2, wild-type growth was restored to ΔyopM Y. pestis in both organs. In spleen, the Gr1+ cells differentially recruited by parent and ΔyopM Y. pestis infections were CCR2+ Gr1+ CD11b+ CD11cLo-Int MAC3+ iNOS+ (inducible nitric oxide synthase-positive) inflammatory dendritic cells (iDCs), and their recruitment to spleen from blood was blocked when YopM was present in the infecting strain. Consistent with influx of iDCs being affected by YopM in spleen, the growth defect of the ΔyopM mutant was relieved by the parentY. pestis strain in a coinfection assay in which the parent strain could affect the fate of the mutant intrans . In a mouse model of bubonic plague, CCR2 also was shown to be required for ΔyopM Y. pestis to show wild-type growth in skin. The data imply that YopM's pathogenic effect indirectly undermines signaling through CCR2. We propose a model for how YopM exerts its different effects in liver and spleen.

Distinct CCR2+Gr1+Cells Control Growth of theYersinia pestisΔyopMMutant in Liver and Spleen during Systemic Plague

Distinct CCR2⁺Gr1⁺Cells Control Growth of theYersinia pestisΔyopMMutant in Liver and Spleen during Systemic Plague