Yersinia enterocolitica YopH-Deficient Strain Activates Neutrophil Recruitment to Peyer's Patches and Promotes Clearance of the Virulent Strain

Dave, Mabel N; Silva, Juan Eduardo; Eliçabe, Ricardo Javier; Jeréz, María Belén; Filippa, Verónica; Gorlino, Carolina; Autenrieth, Stella E.; Autenrieth, Ingo B.; Genaro, María Silvia Di

doi:10.1128/iai.00568-16

Cited by 14 publications

(11 citation statements)

References 57 publications

(67 reference statements)

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“…YopE has been notified to regulate the translocation of effector Yops into host cells [ 72 ]. YopH promotes the inhibition of phagocytosis, inhibits cytokine production by T cells and T-cell proliferation, and prevents the expression of the costimulatory receptor CD86 on B cells [ 73 ]. YopO inhibits phagocytosis by disrupting actin filament regulation processes [ 74 ], and YopT disrupts the actin cytoskeleton of the host cell [ 75 ].…”

Section: Pathogenesis Of Y Enterocolitica Infementioning

confidence: 99%

The Most Important Virulence Markers of Yersinia enterocolitica and Their Role during Infection

Bancerz‐Kisiel

Pieczywek

Łada

et al. 2018

Genes

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Yersinia enterocolitica is the causative agent of yersiniosis, a zoonotic disease of growing epidemiological importance with significant consequences for public health. This pathogenic species has been intensively studied for many years. Six biotypes (1A, 1B, 2, 3, 4, 5) and more than 70 serotypes of Y. enterocolitica have been identified to date. The biotypes of Y. enterocolitica are divided according to their pathogenic properties: the non-pathogenic biotype 1A, weakly pathogenic biotypes 2–5, and the highly pathogenic biotype 1B. Due to the complex pathogenesis of yersiniosis, further research is needed to expand our knowledge of the molecular mechanisms involved in the infection process and the clinical course of the disease. Many factors, both plasmid and chromosomal, significantly influence these processes. The aim of this study was to present the most important virulence markers of Y. enterocolitica and their role during infection.

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Section: Pathogenesis Of Y Enterocolitica Infementioning

confidence: 99%

The Most Important Virulence Markers of Yersinia enterocolitica and Their Role during Infection

Bancerz‐Kisiel

Pieczywek

Łada

et al. 2018

Genes

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“…Y. pseudotuberculosis responds by expressing genes to prevent phagocytosis and counteract iron deprivation and RNS, similar to Y. pestis within dLNs (Sebbane et al, 2006b ; Nuss et al, 2017 ). Y. enterocolitica also actively inhibits neutrophil recruitment by a YopH-dependent mechanism that reduces CXCR2 surface expression on neutrophils (Dave et al, 2016 ). Microcolonies within the lamina propria contain CD4 + T cells and inflammatory macrophage and/or dendritic cell populations, in addition to CD8 + T cells.…”

Section: Yersinia Human Disease Progressionmentioning

confidence: 99%

All Yersinia Are Not Created Equal: Phenotypic Adaptation to Distinct Niches Within Mammalian Tissues

Davis

2018

Front. Cell. Infect. Microbiol.

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Yersinia pseudotuberculosis replicates within mammalian tissues to form clustered bacterial replication centers, called microcolonies. A subset of bacterial cells within microcolonies interact directly with host immune cells, and other subsets of bacteria only interact with other bacteria. This establishes a system where subsets of Yersinia have distinct gene expression profiles, which are driven by their unique microenvironments and cellular interactions. When this leads to alterations in virulence gene expression, small subsets of bacteria can play a critical role in supporting the replication of the bacterial population, and can drive the overall disease outcome. Based on the pathology of infections with each of the three Yersinia species that are pathogenic to humans, it is likely that this specialization of bacterial subsets occurs during all Yersiniae infections. This review will describe the pathology that occurs during infection with each of the three human pathogenic Yersinia, in terms of the structure of bacterial replication centers and the specific immune cell subsets that bacteria interact with, and will also describe the outcome these interactions have or may have on bacterial gene expression.

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“…The effector, YopH, is critical for the colonization and virulence of all three pathogenic Yersinia species, is homologous to eukaryotic protein tyrosine phosphatases (PTPase), and is the most active of all known PTPases [5,[26][27][28][29][30][31][32][33][34][35]. Growth of a Yptb ΔyopH mutant is significantly restored in the absence of neutrophils, indicating that YopH targets antimicrobial functions of neutrophils [36].…”

Section: Introductionmentioning

confidence: 99%

Yersinia pseudotuberculosis YopH targets SKAP2-dependent and independent signaling pathways to block neutrophil antimicrobial mechanisms during infection

et al. 2020

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Yersinia suppress neutrophil responses by using a type 3 secretion system (T3SS) to inject 6-7 Yersinia effector proteins (Yops) effectors into their cytoplasm. YopH is a tyrosine phosphatase that causes dephosphorylation of the adaptor protein SKAP2, among other targets in neutrophils. SKAP2 functions in reactive oxygen species (ROS) production, phagocytosis, and integrin-mediated migration by neutrophils. Here we identify essential neutrophil functions targeted by YopH, and investigate how the interaction between YopH and SKAP2 influence Yersinia pseudotuberculosis (Yptb) survival in tissues. The growth defect of a ΔyopH mutant was restored in mice defective in the NADPH oxidase complex, demonstrating that YopH is critical for protecting Yptb from ROS during infection. The growth of a ΔyopH mutant was partially restored in Skap2-deficient (Skap2KO) mice compared to wildtype (WT) mice, while induction of neutropenia further enhanced the growth of the ΔyopH mutant in both WT and Skap2KO mice. YopH inhibited both ROS production and degranulation triggered via integrin receptor, G-protein coupled receptor (GPCR), and Fcγ receptor (FcγR) stimulation. SKAP2 was required for integrin receptor and GPCR-mediated ROS production, but dispensable for degranulation under all conditions tested. YopH blocked SKAP2-independent FcγR-stimulated phosphorylation of the proximal signaling proteins Syk, SLP-76, and PLCγ2, and the more distal signaling protein ERK1/2, while only ERK1/2 phosphorylation was dependent on SKAP2 following integrin receptor activation. These findings reveal that YopH prevents activation of both SKAP2-dependent and-independent neutrophilic defenses, uncouple integrin-and GPCR-dependent ROS production from FcγR responses based on their SKAP2 dependency, and show that SKAP2 is not required for degranulation.

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Yersinia enterocolitica YopH-Deficient Strain Activates Neutrophil Recruitment to Peyer's Patches and Promotes Clearance of the Virulent Strain

Cited by 14 publications

References 57 publications

The Most Important Virulence Markers of Yersinia enterocolitica and Their Role during Infection

The Most Important Virulence Markers of Yersinia enterocolitica and Their Role during Infection

All Yersinia Are Not Created Equal: Phenotypic Adaptation to Distinct Niches Within Mammalian Tissues

Yersinia pseudotuberculosis YopH targets SKAP2-dependent and independent signaling pathways to block neutrophil antimicrobial mechanisms during infection

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