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

Ye, Zhan; Uittenbogaard, Annette; Cohen, Donald A.; Kaplan, Alan M.; Ambati, Jayakrishna; Straley, Susan C.

doi:10.1128/iai.00808-10

Cited by 24 publications

(57 citation statements)

References 63 publications

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“…1E). These results are consistent with the recent observation of trans-complementation occurring in the spleens (but not the livers) of mice inoculated intravenous with Y. pestis KIM5 (pgm − ) and an isogenic ΔyopM mutant (15). Although trans-complementation following subcutaneous or intravenous infection are not as pronounced as that seen during pulmonary coinfection, all of these results suggest a dominant immunosuppressive effect of wild-type bacteria and demonstrate that the physiology of different organ systems may determine the extent of trans-complementation.…”

Section: Resultssupporting

confidence: 81%

Pulmonary infection by Yersinia pestis rapidly establishes a permissive environment for microbial proliferation

Price

Jin

Goldman³

2012

Proc. Natl. Acad. Sci. U.S.A.

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Disease progression of primary pneumonic plague is biphasic, consisting of a preinflammatory and a proinflammatory phase. During the long preinflammatory phase, bacteria replicate to high levels, seemingly uninhibited by normal pulmonary defenses. In a coinfection model of pneumonic plague, it appears that Yersinia pestis quickly creates a localized, dominant anti-inflammatory state that allows for the survival and rapid growth of both itself and normally avirulent organisms. Yersinia pseudotuberculosis, the relatively recent progenitor of Y. pestis, shows no similar trans-complementation effect, which is unprecedented among other respiratory pathogens. We demonstrate that the effectors secreted by the Ysc type III secretion system are necessary but not sufficient to mediate this apparent immunosuppression. Even an unbiased negative selection screen using a vast pool of Y. pestis mutants revealed no selection against any known virulence genes, demonstrating the transformation of the lung from a highly restrictive to a generally permissive environment during the preinflammatory phase of pneumonic plague.inflammation | pathogenesis

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Section: Resultssupporting

confidence: 81%

Pulmonary infection by Yersinia pestis rapidly establishes a permissive environment for microbial proliferation

Price

Jin

Goldman³

2012

Proc. Natl. Acad. Sci. U.S.A.

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“…Both the yopE and yopK mutants have been shown previously to reach MLNs before being cleared (20,25,42), but not at the early time points observed here in the absence of PMNs. These findings are in accordance with those of previous studies using PMN-depleted mice, showing that Y. pseudotuberculosis yopK and yopH mutants, and also Y. pestis yopM mutants, have higher infectious capacities in the absence of PMNs (20,37,38).…”

Section: Discussionsupporting

confidence: 83%

“…In a recent study, we showed that depletion of Gr-1 ϩ cells enables the otherwise avirulent Y. pseudotuberculosis yopK mutant to cause systemic infection in mice (20). Further, Y. pestis grows better in the spleen and liver upon depletion of Gr-1 ϩ cells, and a Y. pestis yopM mutant is more virulent after depletion of either Gr-1 ϩ or Ly6G ϩ cells (37,38). However, the effects of PMN depletion on early infection have not been investigated previously.…”

mentioning

confidence: 99%

“…Anti-Gr-1 recognizes both Ly6G and Ly6C and therefore depletes monocytes in addition to PMNs (36). These antibody depletion models have been used previously to study the role of PMNs during infections with wild-type (wt) bacteria of different Yersinia species and with certain yop mutants (14,20,37,38). In a recent study, we showed that depletion of Gr-1 ϩ cells enables the otherwise avirulent Y. pseudotuberculosis yopK mutant to cause systemic infection in mice (20).…”

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confidence: 99%

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Yersinia pseudotuberculosis Efficiently Escapes Polymorphonuclear Neutrophils during Early Infection

2014

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The human-pathogenic species of the Gram-negative genus Yersinia preferentially target and inactivate cells of the innate immune defense, suggesting that this is a critical step by which these bacteria avoid elimination and cause disease. In this study, bacterial interactions with dendritic cells, macrophages, and polymorphonuclear neutrophils (PMNs) in intestinal lymphoid tissues during early Yersinia pseudotuberculosis infection were analyzed. Wild-type bacteria were shown to interact mainly with dendritic cells, but not with PMNs, on day 1 postinfection, while avirulent yopH and yopE mutants interacted with PMNs as well as with dendritic cells. To unravel the role of PMNs during the early phase of infection, we depleted mice of PMNs by using an anti-Ly6G antibody, after which we could see more-efficient initial colonization by the wild-type strain as well as by yopH, yopE, and yopK mutants on day 1 postinfection. Dissemination of yopH, yopE, and yopK mutants from the intestinal compartments to mesenteric lymph nodes was faster in PMN-depleted mice than in undepleted mice, emphasizing the importance of effective targeting of PMNs by these Yersinia outer proteins (Yops). In conclusion, escape from interaction with PMNs due to the action of YopH, YopE, and YopK is a key feature of pathogenic Yersinia species that allows colonization and effective dissemination.

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“…opM plays a dominant role in the infection processes of different Yersinia strains in different host organs (1)(2)(3)(4). The yopM gene sequence was first reported for Yersinia pestis strain KIM5, and subsequently the encoded protein was demonstrated to be a possible virulence factor that mimicked the host homolog human platelet glycoprotein 1b (GPI␣) and influenced platelet aggregation (5-7).…”

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confidence: 99%

Distribution and Evolution of Yersinia Leucine-Rich Repeat Proteins

Huang

Hui

et al. 2016

Infect Immun

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c Leucine-rich repeat (LRR) proteins are widely distributed in bacteria, playing important roles in various protein-protein interaction processes. In Yersinia, the well-characterized type III secreted effector YopM also belongs to the LRR protein family and is encoded by virulence plasmids. However, little has been known about other LRR members encoded by Yersinia genomes or their evolution. In this study, the Yersinia LRR proteins were comprehensively screened, categorized, and compared. The LRR proteins encoded by chromosomes (LRR1 proteins) appeared to be more similar to each other and different from those encoded by plasmids (LRR2 proteins) with regard to repeat-unit length, amino acid composition profile, and gene expression regulation circuits. LRR1 proteins were also different from LRR2 proteins in that the LRR1 proteins contained an E3 ligase domain (NEL domain) in the C-terminal region or an NEL domain-encoding nucleotide relic in flanking genomic sequences. The LRR1 proteinencoding genes (LRR1 genes) varied dramatically and were categorized into 4 subgroups (a to d), with the LRR1a to -c genes evolving from the same ancestor and LRR1d genes evolving from another ancestor. The consensus and ancestor repeat-unit sequences were inferred for different LRR1 protein subgroups by use of a maximum parsimony modeling strategy. Structural modeling disclosed very similar repeat-unit structures between LRR1 and LRR2 proteins despite the different unit lengths and amino acid compositions. Structural constraints may serve as the driving force to explain the observed mutations in the LRR regions. This study suggests that there may be functional variation and lays the foundation for future experiments investigating the functions of the chromosomally encoded LRR proteins of Yersinia.

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

Abstract: We are using a systemic plague model to identify the cells and pathways that are undermined by the virulence protein YopM of the plague bacterium Yersinia pestis. In this study, we pursued previous findings that Gr1

Cited by 24 publications

References 63 publications

Pulmonary infection by Yersinia pestis rapidly establishes a permissive environment for microbial proliferation

Pulmonary infection by Yersinia pestis rapidly establishes a permissive environment for microbial proliferation

Yersinia pseudotuberculosis Efficiently Escapes Polymorphonuclear Neutrophils during Early Infection

Distribution and Evolution of Yersinia Leucine-Rich Repeat Proteins

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