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The dynamics of T cells during persistent Staphylococcus aureus infection: from antigen-reactivity to in vivo anergy.

Ziegler C, Goldmann O, Hobeika E, Geffers R, Peters G, Medina E - EMBO Mol Med (2011)

Bottom Line: The mechanisms by which persistent infections are maintained involve both bacterial escape strategies and modulation of the host immune response.So far, the investigations in this area have focused on strategies used by S. aureus to persist within the host.The T cell hyporesponsiveness was reverted by co-stimulation with the phorbol ester PMA, an activator of protein kinase C, suggesting that a failure in the T cell receptor (TCR)-proximal signalling events underlie the hyporesponsive phenotype.

View Article: PubMed Central - PubMed

Affiliation: Infection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.

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H&E-stained sections of kidney tissue collected from mice at day 56 after S. aureus inoculationS. aureus renal abscess with a peripheral fibrin wall (fw). Original magnification, ×20.Cluster of neutrophils occupying the central part of the renal abscess. Original magnification, ×63.Rim of apoptotic neutrophils. Original magnification, ×63.External layer of B and T cells. Original magnification, ×63. The inset in the upper right corner displays a high magnification (×100) photograph showing cells with the typical morphology of plasma cells.Collection of staphylococci can be found associated with fibrin strands. Original magnification, ×100.Empty spaces or caverns (asterisks) formed after the resolution of abscesses. Original magnification, ×20.
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fig02: H&E-stained sections of kidney tissue collected from mice at day 56 after S. aureus inoculationS. aureus renal abscess with a peripheral fibrin wall (fw). Original magnification, ×20.Cluster of neutrophils occupying the central part of the renal abscess. Original magnification, ×63.Rim of apoptotic neutrophils. Original magnification, ×63.External layer of B and T cells. Original magnification, ×63. The inset in the upper right corner displays a high magnification (×100) photograph showing cells with the typical morphology of plasma cells.Collection of staphylococci can be found associated with fibrin strands. Original magnification, ×100.Empty spaces or caverns (asterisks) formed after the resolution of abscesses. Original magnification, ×20.

Mentions: To gain a deeper insight into the local infection process, we performed histopathological examination of kidney tissue obtained at 56 days p.i. As shown in Fig 2A, kidney pathology was characterized by the presence of abscesses, which are a typical pathological feature of staphylococcal infections (Cheng et al, 2009; Lowy, 1998). Renal abscesses comprised an inner accumulation of neutrophils (Fig 2B) and were surrounded by a rim of apoptotic neutrophils (Fig 2C), a peripheral fibrin wall (Fig 2A, fw) and an external layer of B and T cells (Fig 2D). Interestingly, we found collections of staphylococci within the fibrin wall (Fig 2E). This observation suggests that the initiation of abscesses probably involved the deposition of fibrin in response to infection-related inflammation and the sequestration of the staphylococci in the fibrin clot. Eventually, the abscesses resolved leaving empty spaces or caverns in the infected organ (Fig 2F, asterisks).


The dynamics of T cells during persistent Staphylococcus aureus infection: from antigen-reactivity to in vivo anergy.

Ziegler C, Goldmann O, Hobeika E, Geffers R, Peters G, Medina E - EMBO Mol Med (2011)

H&E-stained sections of kidney tissue collected from mice at day 56 after S. aureus inoculationS. aureus renal abscess with a peripheral fibrin wall (fw). Original magnification, ×20.Cluster of neutrophils occupying the central part of the renal abscess. Original magnification, ×63.Rim of apoptotic neutrophils. Original magnification, ×63.External layer of B and T cells. Original magnification, ×63. The inset in the upper right corner displays a high magnification (×100) photograph showing cells with the typical morphology of plasma cells.Collection of staphylococci can be found associated with fibrin strands. Original magnification, ×100.Empty spaces or caverns (asterisks) formed after the resolution of abscesses. Original magnification, ×20.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3377109&req=5

fig02: H&E-stained sections of kidney tissue collected from mice at day 56 after S. aureus inoculationS. aureus renal abscess with a peripheral fibrin wall (fw). Original magnification, ×20.Cluster of neutrophils occupying the central part of the renal abscess. Original magnification, ×63.Rim of apoptotic neutrophils. Original magnification, ×63.External layer of B and T cells. Original magnification, ×63. The inset in the upper right corner displays a high magnification (×100) photograph showing cells with the typical morphology of plasma cells.Collection of staphylococci can be found associated with fibrin strands. Original magnification, ×100.Empty spaces or caverns (asterisks) formed after the resolution of abscesses. Original magnification, ×20.
Mentions: To gain a deeper insight into the local infection process, we performed histopathological examination of kidney tissue obtained at 56 days p.i. As shown in Fig 2A, kidney pathology was characterized by the presence of abscesses, which are a typical pathological feature of staphylococcal infections (Cheng et al, 2009; Lowy, 1998). Renal abscesses comprised an inner accumulation of neutrophils (Fig 2B) and were surrounded by a rim of apoptotic neutrophils (Fig 2C), a peripheral fibrin wall (Fig 2A, fw) and an external layer of B and T cells (Fig 2D). Interestingly, we found collections of staphylococci within the fibrin wall (Fig 2E). This observation suggests that the initiation of abscesses probably involved the deposition of fibrin in response to infection-related inflammation and the sequestration of the staphylococci in the fibrin clot. Eventually, the abscesses resolved leaving empty spaces or caverns in the infected organ (Fig 2F, asterisks).

Bottom Line: The mechanisms by which persistent infections are maintained involve both bacterial escape strategies and modulation of the host immune response.So far, the investigations in this area have focused on strategies used by S. aureus to persist within the host.The T cell hyporesponsiveness was reverted by co-stimulation with the phorbol ester PMA, an activator of protein kinase C, suggesting that a failure in the T cell receptor (TCR)-proximal signalling events underlie the hyporesponsive phenotype.

View Article: PubMed Central - PubMed

Affiliation: Infection Immunology Research Group, Helmholtz Centre for Infection Research, Braunschweig, Germany.

Show MeSH
Related in: MedlinePlus