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Immunodepression in the surgical patient and increased susceptibility to infection.

Volk HD - Crit Care (2002)

View Article: PubMed Central - PubMed

Affiliation: Institute of Clinical Immunology, Charité, Humboldt University Berlin, Berlin, Germany. hans-dieter.volk@charite.de

ABSTRACT

Multiple organ failure is the major problem in intensive care patients. The failure of the organ 'immune system' is frequently overlooked, however. In this issue the article by Angele and Faist provides an excellent review of the topic. Deactivation of monocyte and lymphocyte functions seems to play a key role in post-traumatic immunodepression. To accompany that review we summarize our knowledge of the mechanisms of deactivation. Stress response, lipopolysaccharide translocalization and tissue injury contribute to 'immunoparalysis'. Recently developed, well standardized assays now allow us to monitor the immune system like other organ functions and opens new approaches for therapeutic interventions.

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Related in: MedlinePlus

Regulation of monocytic HLA-DR, tumour necrosis factor (TNF) secretion and antigen-presenting cell (APC) activity. G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte/macrophage colony-stimulating factor; IFN, interferon; LPS, lipopolysaccharide; TGF, transforming growth factor.
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Figure 1: Regulation of monocytic HLA-DR, tumour necrosis factor (TNF) secretion and antigen-presenting cell (APC) activity. G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte/macrophage colony-stimulating factor; IFN, interferon; LPS, lipopolysaccharide; TGF, transforming growth factor.

Mentions: Activation of the stress response plays an important role in downregulating systemic immune responsiveness following trauma, injury and blood loss (Fig. 1). The regulatory role of the hypothalamic-pituitary-adrenal axis, which can stimulate corticosteroid release, is well established. Recent data [2,3] show that the sympathetic nerve system and the vagus are also involved in the regulation of immune responsiveness. The three systems downregulate monocyte/macrophage proinflammatory (e.g. TNF release) and antigen-presenting functions both directly and indirectly by induction of immunomodulatory cytokines (e.g. IL-10). IL-10 also deactivates T cells, in particular type 1 cytokine-secreting T cells.


Immunodepression in the surgical patient and increased susceptibility to infection.

Volk HD - Crit Care (2002)

Regulation of monocytic HLA-DR, tumour necrosis factor (TNF) secretion and antigen-presenting cell (APC) activity. G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte/macrophage colony-stimulating factor; IFN, interferon; LPS, lipopolysaccharide; TGF, transforming growth factor.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC137302&req=5

Figure 1: Regulation of monocytic HLA-DR, tumour necrosis factor (TNF) secretion and antigen-presenting cell (APC) activity. G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocyte/macrophage colony-stimulating factor; IFN, interferon; LPS, lipopolysaccharide; TGF, transforming growth factor.
Mentions: Activation of the stress response plays an important role in downregulating systemic immune responsiveness following trauma, injury and blood loss (Fig. 1). The regulatory role of the hypothalamic-pituitary-adrenal axis, which can stimulate corticosteroid release, is well established. Recent data [2,3] show that the sympathetic nerve system and the vagus are also involved in the regulation of immune responsiveness. The three systems downregulate monocyte/macrophage proinflammatory (e.g. TNF release) and antigen-presenting functions both directly and indirectly by induction of immunomodulatory cytokines (e.g. IL-10). IL-10 also deactivates T cells, in particular type 1 cytokine-secreting T cells.

View Article: PubMed Central - PubMed

Affiliation: Institute of Clinical Immunology, Charité, Humboldt University Berlin, Berlin, Germany. hans-dieter.volk@charite.de

ABSTRACT

Multiple organ failure is the major problem in intensive care patients. The failure of the organ 'immune system' is frequently overlooked, however. In this issue the article by Angele and Faist provides an excellent review of the topic. Deactivation of monocyte and lymphocyte functions seems to play a key role in post-traumatic immunodepression. To accompany that review we summarize our knowledge of the mechanisms of deactivation. Stress response, lipopolysaccharide translocalization and tissue injury contribute to 'immunoparalysis'. Recently developed, well standardized assays now allow us to monitor the immune system like other organ functions and opens new approaches for therapeutic interventions.

Show MeSH
Related in: MedlinePlus