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EcoSal Plus

Domain 8:

Pathogenesis

Cytokines in Salmonellosis

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  • Authors: Pietro Mastroeni1, and Clare Bryant2
  • Editor: Michael S. Donnenberg3
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Bacterial Infection Group, Centre for Veterinary Science, Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 OES, United Kingdom; 2: Bacterial Infection Group, Centre for Veterinary Science, Department of Veterinary Medicine, University of Cambridge, Madingley Road, Cambridge CB3 OES, United Kingdom; 3: University of Maryland, School of Medicine, Baltimore, MD
  • Received 17 June 2004 Accepted 07 September 2004 Published 29 December 2004
  • Address correspondence to Pietro Mastroeni pm274@cam.ac.uk and Clare Bryant ceb27@cam.ac.uk.
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  • Abstract:

    The recruitment and activation of phagocytic cells in infected tissues and the induction of T-cell- and B-cell-dependent acquired immunity are crucial for the control and resolution of infections. These complex processes require the interaction of bacteria with a multitude of cell surface receptors and the controlled production of soluble mediators. The mechanisms of cytokine induction in response to and the role of cytokine networks in infections are the main foci of this review. Pathogen-associated molecular pattern receptors play an important role in recognition of bacteria by the host. Effective immunity against the bacterium therefore relies on the ability of the host to recruit phagocytes in the tissues and to enhance the antibacterial functions of these inflammatory cells. TNF-a, IFN-?, IL12, IL15, and IL18 are needed for the full expression of innate host resistance to . The genes for mammalian cytokines can be cloned into suitable vectors and expressed in as functional proteins. The in vivo production of cytokines by carriers can have therapeutic applications and can modulate immune functions in the host. The possibility to modulate antigen-specific immune responses by expressing cytokines in is illustrated by the increase in -specific IgA responses induced by administration of IL-5-expressing bacteria. The same cytokines that are responsible for endotoxic shock are elevated in the late stages of lethal infections, indicating that the toxicity of lipopolysaccharide (LPS) may actually be contributing to the death of the host.

  • Citation: Mastroeni P, Bryant C. 2004. Cytokines in Salmonellosis, EcoSal Plus 2004; doi:10.1128/ecosalplus.8.8.5

Key Concept Ranking

Tumor Necrosis Factor alpha
0.46288016
Transforming Growth Factor beta
0.4380673
Bacterial Proteins
0.40134928
0.46288016

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ecosalplus.8.8.5.citations
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/content/journal/ecosalplus/10.1128/ecosalplus.8.8.5
2004-12-29
2017-04-27

Abstract:

The recruitment and activation of phagocytic cells in infected tissues and the induction of T-cell- and B-cell-dependent acquired immunity are crucial for the control and resolution of infections. These complex processes require the interaction of bacteria with a multitude of cell surface receptors and the controlled production of soluble mediators. The mechanisms of cytokine induction in response to and the role of cytokine networks in infections are the main foci of this review. Pathogen-associated molecular pattern receptors play an important role in recognition of bacteria by the host. Effective immunity against the bacterium therefore relies on the ability of the host to recruit phagocytes in the tissues and to enhance the antibacterial functions of these inflammatory cells. TNF-a, IFN-?, IL12, IL15, and IL18 are needed for the full expression of innate host resistance to . The genes for mammalian cytokines can be cloned into suitable vectors and expressed in as functional proteins. The in vivo production of cytokines by carriers can have therapeutic applications and can modulate immune functions in the host. The possibility to modulate antigen-specific immune responses by expressing cytokines in is illustrated by the increase in -specific IgA responses induced by administration of IL-5-expressing bacteria. The same cytokines that are responsible for endotoxic shock are elevated in the late stages of lethal infections, indicating that the toxicity of lipopolysaccharide (LPS) may actually be contributing to the death of the host.

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Figures

Image of Figure 1
Figure 1

Red arrows and red text indicate activation pathways. Black arrows and black text indicate inhibitory pathways. Salmonellae infect resident macrophages (RM) and induce production of TNF-α, IL-12, and IL-18 from these cells. TNF-α mediates the recruitment of inflammatory macrophages (IM) in the tissues and the formation of granulomas. IL-12 and IL-18 trigger IFN-γ production from NK cells. IFN-γ activates macrophages, increasing their antibacterial functions. IL-4 production by NK1.1 TCR cells as a consequence of interactions with macrophages (probably via CD1 molecules) can exert a negative effect on macrophage functions. IL-10 can also potentially counteract macrophage activation by IFN-γ. IL-10 and IL-4 production is down-regulated by IL-12 and IFN-γ.

Citation: Mastroeni P, Bryant C. 2004. Cytokines in Salmonellosis, EcoSal Plus 2004; doi:10.1128/ecosalplus.8.8.5
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