Interferon Gamma-1b in the Treatment of Compensatory Anti-inflammatory Response Syndrome

Kox, Wolfgang J.; Bone, Roger C.; Krausch, Dietmar; Döcke, W D; Kox, S N; Wauer, Helmar; Egerer, Karl; Querner, S; Asadullah, Khusru; Baehr, R. von; Volk, H. D.

doi:10.1001/archinte.1997.00440250031004

Cited by 129 publications

(15 citation statements)

References 31 publications

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“…In contrast to TNF-a, IFN-g levels did not correlate with disease severity [23]. Recent reports imply that IFN-g is more involved in compensatory anti-inflammatory response syndrome rather than SIRS [24,25]. Furthermore, careful study of Fig.…”

Section: Discussionmentioning

confidence: 86%

Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome

et al. 2001

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Section: Discussionmentioning

confidence: 86%

Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome

et al. 2001

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“…Impairment of IFN-γ production is a hallmark of the altered immune function that follows sepsis and trauma [3,4]. Some clinical trials have shown that administration of IFN-γ to trauma and high-risk surgical patients will improve immune function, increase resistance to infection and, in some cases, enhance survival [4][5][6]. Expression of IFN-γ is regulated, in part, by the macrophage-derived cytokines interleukin-12 (IL-12) and IL-18 [3,7].…”

Section: Introductionmentioning

confidence: 99%

Glucan phosphate potentiates endotoxin-induced interferon-γ expression in immunocompetent mice, but attenuates induction of endotoxin tolerance

et al. 2001

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Glucan phosphate has been shown to enhance antimicrobial immunity in a variety of experimental models. However, the mechanisms by which glucans enhance resistance to infection remain largely unknown. Interferon-gamma (IFN-gamma) is a key regulator of both innate and acquired immunity. Suppression of IFN-gamma production is a prominent feature of the altered immune response that follows major trauma or sepsis. The present studies were designed to determine the effect of glucan phosphate on IFN-gamma expression in normal mice and endotoxin [lipopolysaccharide (LPS)]-tolerant mice. The model of LPS tolerance was used because it results in patterns of cytokine expression similar to those commonly observed following severe trauma or sepsis. Glucan treatment potentiated LPS-induced IFN-gamma expression in control mice. The induction of LPS tolerance resulted in marked suppression of LPS-induced IFN-gamma production. However, co-administration of glucan with LPS, during the tolerance induction phase, attenuated the LPS-tolerant response. Interleukin-12 (IL-12) and IL-18 are important mediators of LPS-induced IFN-gamma production. LPS-induced IL-12 p40 mRNA expression was increased in the spleens of glucan-treated mice compared with controls. Induction of LPS tolerance caused marked suppression of IL-12 production, a response that was attenuated by glucan treatment. IL-18 was constitutively expressed in both control and LPS-tolerant mice, and LPS-induced serum levels of IL-18 were increased in mice treated with glucan. T cells isolated from glucan-treated mice exhibited increased IFN-gamma expression in response to IL-12 and IL-18, as well as increased expression of the IL-12 and IL-18 receptors. The ability of glucan to potentiate IFN-gamma expression in control mice provides a potential mechanism by which glucan enhances antimicrobial immunity. The ability of glucan to attenuate suppressed IFN-gamma expression in LPS-tolerant mice denotes its potential benefit for the treatment of trauma and sepsis-induced immunosuppression.

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“…The monocytes of these patients were found to have a profound reduction in HLA-DR expression and a reduced ability to produce lipopolysaccharide (LPS)-induced TNF-a in vitro. Exogenous administration of interferon gamma (IFN-g) increased HLA-DR expression to normal levels [7,21] and simultaneously restored the monocyte capacity to produce TNF-a upon LPS stimulation [7]. This series of events, triggered by the administration of IFN-g, was accompanied by resolution of the infection in eight out of the nine septic patients in a pilot clinical study [7].…”

mentioning

confidence: 99%

Paralysed monocytes in acute on chronic liver disease

Antoniades

Wendon

Vergani

2005

Journal of Hepatology

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Interferon Gamma-1b in the Treatment of Compensatory Anti-inflammatory Response Syndrome

Cited by 129 publications

References 31 publications

Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome

Macrophage migration inhibitory factor is a critical mediator of systemic inflammatory response syndrome

Glucan phosphate potentiates endotoxin-induced interferon-γ expression in immunocompetent mice, but attenuates induction of endotoxin tolerance

Paralysed monocytes in acute on chronic liver disease

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