Interferon‐γ in healthy subjects: selective modulation of inflammatory mediators

Metz, Jesse de; Hack, C. E.; Romijn, Johannes A.; Levi, Marcel; Out, Theo A.; Berge, Ineke J. M. ten; Sauerwein, Hans P.

doi:10.1046/j.1365-2362.2001.00833.x

Cited by 14 publications

(12 citation statements)

References 53 publications

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“…In most of the studies exploring IL-8 levels in biological fluids, lower IL-8 concentrations have been detected compared to those used in the present study [42,43]. However, our results are in line with data obtained by Itoh et al [12], who observed a significant IL-8-induced cell proliferation at the same IL-8 concentrations utilized in our study.…”

Section: Discussionsupporting

confidence: 92%

Interleukin-8 stimulates cell proliferation in non-small cell lung cancer through epidermal growth factor receptor transactivation

et al. 2007

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Section: Discussionsupporting

confidence: 92%

Interleukin-8 stimulates cell proliferation in non-small cell lung cancer through epidermal growth factor receptor transactivation

et al. 2007

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“…Two possible explanations could be provided for these differences in plasma. First, IFN-γ treatment has been shown to decrease levels of PAI-1 in healthy controls [43,44]. Since interferon production in patients with asthma has been shown to be impaired [45-47] this might explain the increased levels of PAI-1 in the present study.…”

Section: Discussionmentioning

confidence: 73%

Evaluation of coagulation activation after Rhinovirus infection in patients with asthma and healthy control subjects: an observational study

Majoor¹,

Pol²,

Kamphuisen³

et al. 2014

Respir Res

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BackgroundAsthma exacerbations are frequently triggered by rhinovirus infections. Both asthma and respiratory tract infection can activate haemostasis. Therefore we hypothesized that experimental rhinovirus-16 infection and asthmatic airway inflammation act in synergy on the haemostatic balance.Methods28 patients (14 patients with mild allergic asthma and 14 healthy non-allergic controls) were infected with low-dose rhinovirus type 16. Venous plasma and bronchoalveolar lavage fluid (BAL fluid) were obtained before and 6 days after infection to evaluate markers of coagulation activation, thrombin-antithrombin complexes, von Willebrand factor, plasmin-antiplasmin complexes, plasminogen activator inhibitor type-1, endogenous thrombin potential and tissue factor-exposing microparticles by fibrin generation test, in plasma and/or BAL fluid. Data were analysed by nonparametric tests (Wilcoxon, Mann Whitney and Spearman correlation).Results13 patients with mild asthma (6 females, 19-29 y) and 11 healthy controls (10 females, 19-31 y) had a documented Rhinovirus-16 infection. Rhinovirus-16 challenge resulted in a shortening of the fibrin generation test in BAL fluid of asthma patients (t = -1: 706 s vs. t = 6: 498 s; p = 0.02), but not of controls (t = -1: 693 s vs. t = 6: 636 s; p = 0.65). The fold change in tissue factor-exposing microparticles in BAL fluid inversely correlated with the fold changes in eosinophil cationic protein and myeloperoxidase in BAL fluid after virus infection (r = -0.517 and -0.528 resp., both p = 0.01).Rhinovirus-16 challenge led to increased plasminogen activator inhibitor type-1 levels in plasma in patients with asthma (26.0 ng/mL vs. 11.5 ng/mL in healthy controls, p = 0.04). Rhinovirus-16 load in BAL showed a linear correlation with the fold change in endogenous thrombin potential, plasmin-antiplasmin complexes and plasminogen activator inhibitor type-1.ConclusionsExperimental rhinovirus infection induces procoagulant changes in the airways of patients with asthma through increased activity of tissue factor-exposing microparticles. These microparticle-associated procoagulant changes are associated with both neutrophilic and eosinophilic inflammation. Systemic activation of haemostasis increases with Rhinoviral load.Trial registrationThis trial was registered at the Dutch trial registry (http://www.trialregister.nl): NTR1677.

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“…It is rapidly induced and secreted by NK cells after pathogen encounter by the host. Furthermore, macrophage and neutrophil activation by IFN-␥ results in the secretion of tumor necrosis factor alpha (64) and reactive oxygen intermediates (18,19,30). Thus, IFN-␥ is a key mediator of inflammatory responses (8,25).…”

mentioning

confidence: 99%

Gamma Interferon-Mediated Inflammation Is Associated with Lack of Protection from Intravaginal Simian Immunodeficiency Virus SIVmac239 Challenge in Simian-Human Immunodeficiency Virus 89.6-Immunized Rhesus Macaques

Abel

Franco-Scheuch

Rourke

et al. 2004

J Virol

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Interferon‐γ in healthy subjects: selective modulation of inflammatory mediators

Abstract: We conclude that IFN-gamma selectively affects host inflammatory mediators in humans.

Cited by 14 publications

References 53 publications

Interleukin-8 stimulates cell proliferation in non-small cell lung cancer through epidermal growth factor receptor transactivation

Interleukin-8 stimulates cell proliferation in non-small cell lung cancer through epidermal growth factor receptor transactivation

Evaluation of coagulation activation after Rhinovirus infection in patients with asthma and healthy control subjects: an observational study

Gamma Interferon-Mediated Inflammation Is Associated with Lack of Protection from Intravaginal Simian Immunodeficiency Virus SIVmac239 Challenge in Simian-Human Immunodeficiency Virus 89.6-Immunized Rhesus Macaques

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