Release of interleukin-1 by peripheral blood mononuclear cells in patients with tuberculosis and active inflammation

Chensue, Stephen W.; Davey, Michael P.; Remick, Daniel G.; Kunkel, S L

doi:10.1128/iai.52.1.341-343.1986

Cited by 39 publications

(8 citation statements)

References 7 publications

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“…136 Recent studies suggest that the data obtained with granulomatous animal models may be applicable to humans. Monocytes from patients with leprosy and tuberculosis spontaneously produce IL-1like activity 143 and the alveolar macrophages from patients with sarcoidosis produce exaggerated amounts of IL-1. [144][145][146][147][148] IL-1 also has been detected histologically in sarcoidosis granulomas, 149 and the bronchoalveolar lavage (BAL) fluid of patients with sarcoidosis has been reported to contain a factor that augments macrophage IL-1-ß production.…”

Section: Interleukin-1mentioning

confidence: 99%

Cytokines and Cytokine Networking in the Pathogenesis of Interstitial and Fibrotic Lung Disorders

Rochester¹,

Jack²

1993

Semin Respir Crit Care Med

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Section: Interleukin-1mentioning

confidence: 99%

Cytokines and Cytokine Networking in the Pathogenesis of Interstitial and Fibrotic Lung Disorders

Rochester¹,

Jack²

1993

Semin Respir Crit Care Med

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“…As a result, the production of this cytokine must be repressed in chronically Mtb-infected animals to avoid progressive pathology [21] , [29] . While, production of IL-1β correlates with the severity of human TB disease [30] , [31] , its paradoxical activities in promoting both antimycobacterial immunity and chronic tissue damage leave the ultimate contribution of this cytokine to TB progression in human populations unclear.…”

Section: Introductionmentioning

confidence: 99%

Allele-Specific Induction of IL-1β Expression by C/EBPβ and PU.1 Contributes to Increased Tuberculosis Susceptibility

Zhang

Zhou

et al. 2014

PLoS Pathog

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Mycobacterium tuberculosis infection is associated with a spectrum of clinical outcomes, from long-term latent infection to different manifestations of progressive disease. Pro-inflammatory pathways, such as those controlled by IL-1β, have the contrasting potential both to prevent disease by restricting bacterial replication, and to promote disease by inflicting tissue damage. Thus, the ultimate contribution of individual inflammatory pathways to the outcome of M. tuberculosis infection remains ambiguous. In this study, we identified a naturally-occurring polymorphism in the human IL1B promoter region, which alters the association of the C/EBPβ and PU.1 transcription factors and controls Mtb-induced IL-1β production. The high-IL-1β expressing genotype was associated with the development of active tuberculosis, the severity of pulmonary disease and poor treatment outcome in TB patients. Higher IL-1β expression did not suppress the activity of IFN-γ-producing T cells, but instead correlated with neutrophil accumulation in the lung. These observations support a specific role for IL-1β and granulocytic inflammation as a driver of TB disease progression in humans, and suggest novel strategies for the prevention and treatment of tuberculosis.

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“…Among them Mycobacterium tuberculosis ‐specific serum antibodies, the T‐lymphocyte enzyme adenosine deaminase, the macrophage activation product neopterin, the mononuclear cell surface protein β 2 microglobulin, soluble T‐cell interleukin (IL)‐2 receptors as well as soluble CD4 and CD8 receptors, macrophage and T‐cell adhesion molecules and acute phase reactant proteins have all been proposed as indicators of disease activity in pulmonary and extrapulmonary TB [1–5] and as diagnostic and prognostic indicators in tuberculous pleural effusions [6]. More recently, the cytokines tumour necrosis factor (TNF‐α), IL‐1, IL‐6, interferon gamma (IFN‐γ) and IL‐12 and the chemokines IL‐8, monocyte chemotactic peptide‐1 (MCP‐1) and regulated on activation, normal T cell expressed and secreted (RANTES) have been found to be elevated in the bronchoalveolar lavage fluid or serum of patients with active disease and have been proposed as markers of disease activity [7–12]. However, none of these markers has shown itself as unarguably better than the measurement of haemoglobin concentration and of erythrocyte sedimentation rate, which are the most inexpensive and generally used inflammation markers.…”

mentioning

confidence: 99%

Soluble immunological markers of disease activity in tuberculosis

Saltini¹,

Colizzi²

1999

Eur Respir J

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The obtention of a microbiologically confirmed diagnosis of tuberculosis (TB), assessment of the extent and intensity of disease activity, and follow-up of the patient response to treatment are all encumbered by our still limited ability to quantify the infectious load using the microbiological tools available in current practice. In this context, a number of attempts have been made to determine the role that soluble disease markers could play as diagnostic and prognostic indicators in pulmonary, pleural and extrapulmonary TB. As in other lung diseases, molecules which become overexpressed during immune cell activation have been measured in biological fluids such as serum, pleural fluid and the epithelial lining fluid (ELF) of the lower respiratory tract of TB patients, with the intent of gauging the activation of the immune system in response to the TB bacillus, to assess disease activity and predict the disease course.A number of specific and nonspecific immune marker studies have thus appeared in the literature in the last twenty years. Among them Mycobacterium tuberculosis-specific serum antibodies, the T-lymphocyte enzyme adenosine deaminase, the macrophage activation product neopterin, the mononuclear cell surface protein b 2 microglobulin, soluble T-cell interleukin (IL)-2 receptors as well as soluble CD4 and CD8 receptors, macrophage and T-cell adhesion molecules and acute phase reactant proteins have all been proposed as indicators of disease activity in pulmonary and extrapulmonary TB [1±5] and as diagnostic and prognostic indicators in tuberculous pleural effusions [6]. More recently, the cytokines tumour necrosis factor (TNF-a), IL-1, IL-6, interferon gamma (IFN-c) and IL-12 and the chemokines IL-8, monocyte chemotactic peptide-1 (MCP-1) and regulated on activation, normal T cell expressed and secreted (RANTES) have been found to be elevated in the bronchoalveolar lavage fluid or serum of patients with active disease and have been proposed as markers of disease activity [7±12]. However, none of these markers has shown itself as unarguably better than the measurement of haemoglobin concentration and of erythrocyte sedimentation rate, which are the most inexpensive and generally used inflammation markers.By analogy with the other major disease caused by a mycobacterium, leprosy, in which a relationship between the type of immune reaction, the immunopathology and the clinical course has been characterized in the lepromatous and tuberculoid forms of leprosy [13], the identification of immunological markers of the "classic" pathological expressions of disease, i.e. the exudative and productive forms of TB, has been attempted, although not as successfully. Based upon the leprosy model, a spectrum of immunopathological reactions was identified in TB in 1977 [14], whereby the tuberculin reaction and the level of specific antibodies in serum were proposed as the markers of a spectrum of clinical presentations. In that study, the self-limiting course and the good response to chemotherapy of paucibaciliary prod...

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Release of interleukin-1 by peripheral blood mononuclear cells in patients with tuberculosis and active inflammation

Cited by 39 publications

References 7 publications

Cytokines and Cytokine Networking in the Pathogenesis of Interstitial and Fibrotic Lung Disorders

Cytokines and Cytokine Networking in the Pathogenesis of Interstitial and Fibrotic Lung Disorders

Allele-Specific Induction of IL-1β Expression by C/EBPβ and PU.1 Contributes to Increased Tuberculosis Susceptibility

Soluble immunological markers of disease activity in tuberculosis

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