Effect of rLcrV and rYopB from Yersinia pestis on murine peritoneal macrophages in vitro

Sharma, Rajesh; Sodhi, Ajit; Batra, Harsh Vardhan; Tuteja, Urmil

doi:10.1016/j.imlet.2004.03.010

Cited by 11 publications

(5 citation statements)

References 45 publications

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“…In this study, we verified that infection with Y. pseudotuberculosis exerts a suppressor role on TNF-a and IL-12 production by macrophages from BALB ⁄ c and C57BL ⁄ 6 mice, corroborating in vitro studies that reported the function of LcrV and YopB in the inhibition of the production of TNF-a and IL-12 in murine peritoneal macrophages [27] and revealing one survival mechanism used by this bacterium.…”

Section: Discussionsupporting

confidence: 85%

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

Tansini

Medeiros

2009

Scand J Immunol

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T helper 1 cells play a crucial role in the clearance of Yersinia pseudotuberculosis infection. By producing cytokines and presenting antigens to T cells, activated macrophages can orientate the adaptive immune response. The pathway used by macrophages to metabolize arginine has been employed as an important parameter to discriminate their activation state. In this study, the pattern of macrophage activation in Y. pseudotuberculosis-infected BALB ⁄ c (Yersinia-susceptible) and C57BL ⁄ 6 (Yersinia-resistant) mice and their immunostimulatory capacity were analysed. In the early phase of infection, macrophages obtained from C57BL ⁄ 6 mice produced higher levels of NO, lower arginase activity, and larger amounts of IL-12 and TNF-a than macrophages from BALB ⁄ c mice. On the other hand, macrophages derived from BALB ⁄ c mice produced higher levels of IL-10 and TGF-b than C57BL ⁄ 6 mice. The Y. pseudotuberculosis infection leads to a fall in the macrophage immunostimulatory capacity of both strains of mice, with T-cell proliferation significantly reduced 12 h after infection. Moreover, we observed in the supernatant of co-culture of macrophages from infected mice with T lymphocytes from heat-killed Yersiniaimmunized mice lower IFN-c production by cells from BALB ⁄ c mice than by C57BL ⁄ 6 mice, and IL-4 was produced only by BALB ⁄ c mice on the first-and third-day post-infection. These results suggest that the pattern of macrophage activation is associated with susceptibility and resistance to Y. pseudotuberculosis infection in BALB ⁄ c and C57BL ⁄ 6 mice.

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Section: Discussionsupporting

confidence: 85%

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

Tansini

Medeiros

2009

Scand J Immunol

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“…Previous reports suggested that certain Y. pestis proteins may interfere with activation of APCs in vitro (19,20). Therefore, we investigated directly in vivo the effects that infection with the entire Y. pestis organism had on CD11c ϩ airway cells.…”

Section: Y Pestis Infection Induces Rapid Activation Of Cd11cmentioning

confidence: 99%

Early Interaction of Yersinia pestis with APCs in the Lung

Bosio

Goodyear²,

Dow

2005

The Journal of Immunology

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Despite the importance of pneumonic plague, little is known of the early pulmonary immune responses that occur following inhalation of Yersinia pestis. Therefore, we conducted studies to identify the early target cells for uptake of Y. pestis in the lungs following intratracheal or i.v. inoculation. Following intratracheal inoculation, Y. pestis was rapidly internalized primarily by a distinctive population of CD11c+DEC-205+CD11b− cells in the airways, whereas i.v. inoculation resulted in uptake primarily by CD11b+CD11c− macrophages and granulocytes in lung tissues. The airway cells internalized and were infected by Y. pestis, but did not support active replication of the organism. Intratracheal inoculation of Y. pestis resulted in rapid activation of airway CD11c+ cells, followed within 24 h by the selective disappearance of these cells from the airways and lungs and the accumulation of apoptotic CD11c+ cells in draining lymph nodes. When CD11c+ cells in the airways were depleted using liposomal clodronate before infection, this resulted in a significantly increased replication of Y. pestis in the lungs and dissemination to the spleen and draining lymph nodes. These findings suggest that CD11c+ cells in the airways play an important role in suppressing the initial replication and dissemination of inhaled Y. pestis, although these results will also require confirmation using fully virulent strains of Y. pestis. Depletion of these airway cells by Y. pestis may therefore be one strategy the organism uses to overcome pulmonary defenses following inhalation of the organism.

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“…In mice, rV expressed in E. coli inhibited the LPS-induced macrophage production of TNFa, CXCL I0 and IL-12, and treatment of murine macrophages for 2 h with rV resulted in IL-IO expression (22)(23). In our experiments with human monocytes, rFl, rV and rFl-V failed to affect LPSinduced cytokine production, nor up-regulated IL-10.…”

Section: Discussionmentioning

confidence: 46%

“…Since earlier studies reported that V antigen inhibited the LPS-induced TNF-a and IL-12 expression in murine macrophages (22)(23), rF1, rV, and rF I-V were tested for their effects on the LPS-induced cytokine production by human monocytes. At any rF 1, rV, and rF I-V concentration, no significant change was observed in the LPSinduced TNF-a and IL-12 secretion, nor in other cytokines measured in this study (data not shown).…”

Section: Resultsmentioning

confidence: 99%

Plant-Derived Recombinant Fl, V, and F1-V Fusion Antigens ofYersinia PestisActivate Human Cells of the Innate and Adaptive Immune System

Prete

Santi

Andrianaivoarimanana

et al. 2009

Int J Immunopathol Pharmacol

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Plague is still endemic in different regions of the world. Current vaccines raise concern for their side effects and limited protection, highlighting the need for an efficacious and rapidly producible vaccine. Fl and V antigens of Yersinia pestis, and Fl-V fusion protein produced in Nicotiana benthamiana administered to guinea pigs resulted in immunity and protection against an aerosol challenge of virulent Y. pestis. We examined the effects of plant-derived Fl, V, and Fl-V on human cells of the innate immunity. Fl, V, and Fl-V proteins engaged TLR2 signalling and activated IL-6 and CXCL-8 production by monocytes, without affecting the expression ofTNF-a, IL-12, IL-IO, IL-l~, and CXCLIO. Native Fl antigen and recombinant plant-derived Fl (rFl) and rFI-V all induced similar specific T-cell responses, as shown by their recognition by T-cells from subjects who recovered from Y.pestis infection. Native Fl and rFl were equally well recognized by serum antibodies of Y.pestis-primed donors, whereas serological reactivity to rFI-V hybrid was lower, and that to rV was virtually absent. In conclusion, plant-derived Fl, V, and FI-V antigens are weakly reactogenic for human monocytes and elicit cellmediated and humoral responses similar to those raised by Y. pestis infection.Yersinia pestis, the causative agent of plague, is still endemic in Africa, Asia, and the Americas (1). The bubonic form is transmitted via the bite of an infected flea, and bacteria disseminate systemically. The pneumonic form, uniformly fatal, develops from a bubonic state or by aerosol transmission. The control of plague is based on flea control, and chemoprophylaxis of exposed people. The two human vaccines formulated as killed whole cells (KWC) provide little protection against the pneumonic form, have a high incidence of side effects, and require intensive boosting to achieve protection (2). A live attenuated vaccine (EV76) has been used in humans; however, it also causes side effects (3).Recombinant vaccines based on the fraction 1 capsular antigen (F 1), the V antigen, and F I-V fusion protein have proven to be successful in animals and humans (4-5). Fl, encoded on a IIO-kb plasmid (pMT-l), forms a capsule conferring anti-phagocytic properties to Y.

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Effect of rLcrV and rYopB from Yersinia pestis on murine peritoneal macrophages in vitro

Cited by 11 publications

References 45 publications

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

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

Early Interaction of Yersinia pestis with APCs in the Lung

Plant-Derived Recombinant Fl, V, and F1-V Fusion Antigens ofYersinia PestisActivate Human Cells of the Innate and Adaptive Immune System

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