Lung-restricted Activation of the Alveolar Macrophage/Monocyte System in Pulmonary Sarcoidosis

Müller–Quernheim, Joachim; Pfeifer, Sibylle; Männel, Daniela N.; Strausz, J.; Ferlinz, R

doi:10.1164/ajrccm/145.1.187

Cited by 122 publications

(102 citation statements)

References 15 publications

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“…Similar discrepancies exist between studies on cytokine production by sarcoid PBMNC. Some authors have found a decreased production of IL-1β, TNF-α and IL-6 by sarcoid PBMNC and have interpreted this as a consequence of the postulated "anergic state" [22][23][24][25]. Others have detected an enhanced IL-6 generation by sarcoid PBMNC [9,26], which would be in line with the view that these cells are activated [27].…”

Section: Discussionmentioning

confidence: 72%

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Pulmonary sarcoidosis: patterns of cytokine release in vitro

C¹,

Knight²,

Herold³

et al. 1996

Eur Respir J

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This study was designed to investigate the ability of bronchoalveolar and blood mononuclear cells to produce inflammatory mediators in vitro in pulmonary sarcoidosis. Seventeen patients with pulmonary sarcoidosis (stage I n=8; stage II/III n=9) and 10 normal controls were investigated. Bronchoalveolar and peripheral blood mononuclear cells were cultured in serum-free medium, without stimulant, for 24 h, and the supernatants analysed for concentrations of interleukin (IL)-1β (IL-1β), IL-2, IL-6, tumour necrosis factor-α (TNF-α), granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-γ (IFN-γ) and neopterin.Bronchoalveolar lavage cells (BALC) of sarcoid patients released significantly higher amounts of TNF-α, IL-6, IFN-γ and neopterin in comparison to normal controls. When smokers were excluded, there was also an increased release of IL-1β and GM-CSF. In the sarcoid group, the levels of IL-1β, IL-6, TNF-α and GM-CSF showed highly significant correlations between each other, but not with IL-2, IFN-γ or neopterin. Sarcoid patients whose BALC released more TNF-α or GM-CSF had higher percentage counts of alveolar macrophages but fewer lavage lymphocytes. In sarcoid patients, peripheral blood mononuclear cells (PBMNC) also released higher amounts of IL-1β, TNF-α, IL-6 and GM-CSF but less neopterin than normal controls. Patients whose PBMNC produced more IL-1β, IL-6 and GM-CSF had higher absolute and relative lavage neutrophil counts. No relationships were observed between cytokine release and radiographic or physiological markers of disease severity.We conclude from this study that sarcoid inflammation is associated with an increased and concerted release of monocyte/macrophage-derived cytokines not only in the lung but also in the peripheral blood. We speculate that the lymphokines, IFN-γ and IL-2, are not the primary triggers.

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Section: Discussionmentioning

confidence: 72%

“…In some of the studies that failed to detect enhanced cytokine production by sarcoid BALC, bioassays were used for supernatant analysis [19,22], allowing specific inhibitors to interfere with cytokine activity [21,24]. Another bias could result from differences in patient populations regarding disease severity and smoking behaviour.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary sarcoidosis: patterns of cytokine release in vitro

C¹,

Knight²,

Herold³

et al. 1996

Eur Respir J

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“…These previous results indicated that sTNF-R may contribute to regulating TNF--mediated disease. Since TNFhas been suggested to play an important role in the pathogenesis of sarcoidosis [3][4][5][6], one might speculate that sTNF-R in sarcoidosis may contribute to the homeostatic regulation of granuloma formation. Therefore, in addition to estimating the levels of plasma sTNF-R, we also measured plasma TNF-levels and attempted to analyse the relationship between the ratio of plasma sTNF-R levels to plasma TNF-levels and the course of sarcoidosis.…”

Section: Discussionmentioning

confidence: 99%

“…The pathogenesis of sarcoidosis has been extensively investigated, and several inflammatory cells and cytokines play a crucial role in its pathogenesis [1][2][3]. Several studies of macrophage/monocyte-derived cytokines such as IL-1 and TNF-have demonstrated an increased production of these cytokines by unstimulated and stimulated macrophages/monocytes from patients with sarcoidosis [4][5][6]. In addition, the involvement of these cytokines in the formation of granulomata has been shown by employing experimental granulomata and dextran-induced granulomata [7,8].…”

Section: Introductionmentioning

confidence: 99%

Elevation of plasma-soluble tumour necrosis factor receptors (TNF-R) in sarcoidosis

Nakayama

Hashimoto

Amemiya

et al. 1996

Clinical and Experimental Immunology

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SUMMARYTwo types of receptor for tumour necrosis factor-alpha (TNF-R), the 55-kD receptor (TNF-RI) and the 75-kD receptor (TNF-RII), have been identified. Soluble TNF-RI (sTNF-RI) and soluble TNF-RII (sTNF-RII) can be measured in culture supernatants and biological fluids, and the role of sTNF-R has been suggested. In the present study, we measured plasma sTNF-RI and sTNF-RII levels in 19 patients with active sarcoidosis by ELISA in order to assess the state of both types of receptors in this disease. Both plasma sTNF-RI and sTNF-RII levels in patients with active sarcoidosis were significantly higher than those in normal control subjects. A longitudinal evaluation of plasma sTNF-RI and sTNF-RII levels showed that the magnitude of changes in sTNF-RII was closely related with the clinical course of sarcoidosis. These results suggest that plasma sTNF-RII levels may be useful parameters for monitoring the clinical course of sarcoidosis as well as markers for identifying disease activity.

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“…Alveolar macrophages from sarcoidosis patients with active sarcoid secrete large amounts of TNF-␣ [67,68], so there is at least a logical basis for this treatment [69][70][71]. It is often combined with once weekly methotrexate 10 mg per m 2 to reduce antibody formation against infliximab.…”

Section: Treatment Of Sarcoidosis With Infliximabmentioning

confidence: 99%

Paediatric interstitial lung disease

Bush

2005

Breathe

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Key pointsPresentation of ILD is very non-specific.Imaging, especially HRCT, confirms the presence of ILD, but is rarely diagnostic.Invasive diagnosis is almost always needed.Bronchoscopy rarely gives diagnostic information in paediatric ILD.For most paediatric ILD, transbronchial or percutaneous lung biopsy gives insufficient tissue for diagnosis and carries increased risk.Open lung biopsy or VATS is the diagnostic investigation of choice.Educational aimsTo allow the reader to correctly identify infants and children with interstitial lung disease (ILD).To help the reader to appreciate the wide differential diagnosis, including that of disorders specific to infancy, comprising the surfactant protein disorders.To explain the strengths and weaknesses of the different investigative modalities used in establishing a firm diagnosis.To discuss the limited evidence for the different treatment options currently in use.SummaryPaediatric interstitial disease is rare, and comprises many disparate diseases. This article aims to provide the reader with an update on how to recognise infants and children who should be considered as possibly having ILD. The diagnostic process, including the roles of HRCT and bronchoscopy, and the different methods of lung biopsy, will be set out. The newly recognised entities, such as neuroendocrine cell hyperplasia of infancy, pulmonary interstitial glycogenosis and the disorders of surfactant protein metabolism, are also described. Finally, the article reviews the evidence that exists to guide treatment of these conditions.

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Lung-restricted Activation of the Alveolar Macrophage/Monocyte System in Pulmonary Sarcoidosis

Abstract: SUMMARY An activation of T-cells that is

Cited by 122 publications

References 15 publications

Pulmonary sarcoidosis: patterns of cytokine release in vitro

Pulmonary sarcoidosis: patterns of cytokine release in vitro

Elevation of plasma-soluble tumour necrosis factor receptors (TNF-R) in sarcoidosis

Paediatric interstitial lung disease

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