Susceptibility to <i>Yersinia pseudotuberculosis</i> Infection is Linked to the Pattern of Macrophage Activation

Tansini, Aline; Medeiros, Beatriz Maria Machado de

doi:10.1111/j.1365-3083.2008.02212.x

Cited by 3 publications

(3 citation statements)

References 39 publications

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“…Likewise, in the present study we found that YopP inhibited NO production and increased urea levels in a coordinate fashion with Gal1. In agreement with our findings, Silva Monnazzi et al and Tansini et al demonstrated that NO production in murine macrophages is suppressed by Y. pseudotuberculosis and that the YopP counterpart, YopJ, could be, at least in part, responsible of such effect [ 87 , 88 ]. In addition, we observed increased NO production by WT macrophages after inhibition of p38 and ERK1/2 signaling pathways and subsequent infection with Ye wt or Ye ∆ yopP .…”

Section: Discussionsupporting

confidence: 93%

Galectin-1 Cooperates with Yersinia Outer Protein (Yop) P to Thwart Protective Immunity by Repressing Nitric Oxide Production

et al. 2021

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Yersinia enterocolitica (Ye) inserts outer proteins (Yops) into cytoplasm to infect host cells. However, in spite of considerable progress, the mechanisms implicated in this process, including the association of Yops with host proteins, remain unclear. Here, we evaluated the functional role of Galectin-1 (Gal1), an endogenous β-galactoside-binding protein, in modulating Yop interactions with host cells. Our results showed that Gal1 binds to Yops in a carbohydrate-dependent manner. Interestingly, Gal1 binding to Yops protects these virulence factors from trypsin digestion. Given that early control of Ye infection involves activation of macrophages, we evaluated the role of Gal1 and YopP in the modulation of macrophage function. Although Gal1 and YopP did not influence production of superoxide anion and/or TNF by Ye-infected macrophages, they coordinately inhibited nitric oxide (NO) production. Notably, recombinant Gal1 (rGal1) did not rescue NO increase observed in Lgals1−/− macrophages infected with the YopP mutant Ye ∆yopP. Whereas NO induced apoptosis in macrophages, no significant differences in cell death were detected between Gal1-deficient macrophages infected with Ye ∆yopP, and WT macrophages infected with Ye wt. Strikingly, increased NO production was found in WT macrophages treated with MAPK inhibitors and infected with Ye wt. Finally, rGal1 administration did not reverse the protective effect in Peyer Patches (PPs) of Lgals1−/− mice infected with Ye ∆yopP. Our study reveals a cooperative role of YopP and endogenous Gal1 during Ye infection.

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Section: Discussionsupporting

confidence: 93%

Galectin-1 Cooperates with Yersinia Outer Protein (Yop) P to Thwart Protective Immunity by Repressing Nitric Oxide Production

et al. 2021

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“…LcrV-mediated IL-10 production also caused suppression of TNF-␣ production (39). Changes in IL-10 production have also been associated with Y. pseudotuberculosis infection in BALB/c mice (43). A recent publication has demonstrated that IL-10 production is a host response to systemic infection with Y. pestis (35).…”

Section: Discussionmentioning

confidence: 99%

Delineation of Regions of theYersiniaYopM Protein Required for Interaction with the RSK1 and PRK2 Host Kinases and Their Requirement for Interleukin-10 Production and Virulence

2010

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The YopM protein of Yersinia sp. is a type III secreted effector that is required for virulence in murine models of infection. YopM has previously been shown to contain leucine-rich repeats (LRRs) and to interact with two host kinases, RSK1 and PRK2, although the consequence of these interactions is unknown. A series of YopM proteins missing different numbers of LRRs or a C-terminal domain were produced and used for in vitro binding reactions to map domains required for interaction with RSK1 and PRK2. A C-terminal domain of YopM (from LRR12 to the C terminus) was shown to be required for interaction with RSK1, while an internal portion encompassing LRR6 to LRR15 was shown to be required for interaction with PRK2. The virulence of a Yersinia pseudotuberculosis ⌬yopM mutant in mice via an intravenous route of infection was significantly attenuated. At day 4 postinfection, there were significantly increased levels of gamma interferon and reduced levels of interleukin-18 (IL-18) and IL-10 in the serum of the ⌬yopM-infected mice compared to that of mice infected with the wild type, suggesting that YopM action alters the balance of these key cytokines to promote virulence. The PRK2 and RSK1 interaction domains of YopM were both required for IL-10 induction in vivo, irrespective of splenic colonization levels. In an orogastric model of Y. pseudotuberculosis infection, a ⌬yopM mutant was defective in dissemination from the intestine to the spleen and significantly reduced in virulence. In addition, Y. pseudotuberculosis mutants expressing YopM proteins unable to interact with either RSK1 (YopM⌬12-C) or PRK2 (YopM⌬6-15) were defective for virulence in this assay, indicating that both interaction domains are important for YopM to promote pathogenesis.

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“…The plates were incubated with L-arginine (100 µl) at 37°C for 30 min, and then H 2 SO 4 /H 3 PO 4 /H 2 O mixture (800 µl) was added and heated with α-isopropylidene nitrobenzene acetone (50 µl) at 95°C for 30 min. The complex in each well was diluted 20 times with PBS to detect the optical density (OD) values at 540 nm with a UV spectrophotometer [36], [37].…”

Section: Methodsmentioning

confidence: 99%

The Synthetic Melanocortin (CKPV)2 Exerts Anti-Fungal and Anti-Inflammatory Effects against Candida albicans Vaginitis via Inducing Macrophage M2 Polarization

Zou

Duan

et al. 2013

PLoS ONE

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In this study, we examined anti-fungal and anti-inflammatory effects of the synthetic melanocortin peptide (Ac-Cys-Lys-Pro-Val-NH2)2 or (CKPV)2 against Candida albicans vaginitis. Our in vitro results showed that (CKPV)2 dose-dependently inhibited Candida albicans colonies formation. In a rat Candida albicans vaginitis model, (CKPV)2 significantly inhibited vaginal Candida albicans survival and macrophages sub-epithelial mucosa infiltration. For mechanisms study, we observed that (CKPV)2 inhibited macrophages phagocytosis of Candida albicans. Meanwhile, (CKPV)2 administration inhibited macrophage pro-inflammatory cytokines (TNF-α, IL-1β and IL-6) release, while increasing the arginase activity and anti-inflammatory cytokine IL-10 production, suggesting macrophages M1 to M2 polarization. Cyclic AMP (cAMP) production was also induced by (CKPV)2 administration in macrophages. These above effects on macrophages by (CKPV)2 were almost reversed by melanocortin receptor-1(MC1R) siRNA knockdown, indicating the requirement of MC1R in the process. Altogether, our results suggest that (CKPV)2 exerted anti-fungal and anti-inflammatory activities against Candida albicans vaginitis probably through inducing macrophages M1 to M2 polarization and MC1R activation.

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Susceptibility to Yersinia pseudotuberculosis Infection is Linked to the Pattern of Macrophage Activation

Cited by 3 publications

References 39 publications

Galectin-1 Cooperates with Yersinia Outer Protein (Yop) P to Thwart Protective Immunity by Repressing Nitric Oxide Production

Galectin-1 Cooperates with Yersinia Outer Protein (Yop) P to Thwart Protective Immunity by Repressing Nitric Oxide Production

Delineation of Regions of theYersiniaYopM Protein Required for Interaction with the RSK1 and PRK2 Host Kinases and Their Requirement for Interleukin-10 Production and Virulence

The Synthetic Melanocortin (CKPV)2 Exerts Anti-Fungal and Anti-Inflammatory Effects against Candida albicans Vaginitis via Inducing Macrophage M2 Polarization

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