Abnormal Secretion of Interleukin-1 and Tumor Necrosis Factor α by Alveolar Macrophages in Coal Worker's Pneumoconiosis: Comparison between Simple Pneumoconiosis and Progressive Massive Fibrosis

Lassalle, Philippe; Gosset, Philippe; Aerts, C; Fournier, E; Lafitte, J.J.; Degreef, Jean Marc; Wallaert, B.; Tonnel, A. B.; Voisin, C

doi:10.3109/01902149009064700

Cited by 69 publications

(31 citation statements)

References 7 publications

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“…With regard to dust exposure in man, we found that monocyte TNF release upon ex-vivo stimulation with coal dust and silica (and endotoxin) was increased in (retired) miners with or without radiological evidence for simple coal workers pneumoconiosis (CWP) compared to subjects never exposed to mineral dust [3,9]. In line with our observations in monocytes of coal workers, higher TNF secretion was also observed in macrophages of patients with progressive massive fibrosis (PMF) compared to simple pneumoconiosis patients and control subjects [7]. More recently, elevated messenger ribonucleic acid (mRNA) levels of TNF (and IL-6) have been observed in lungs of pneumoconiosis patients [10].…”

supporting

confidence: 80%

“…The pathogenesis of lung fibrosis involves highly complicated processes of intercellular communication by peptides released from and to various immune cells and lung target cells in a phenomenon appropriately referred to as "cytokine network" [2]. Previously, we and others have shown that silica, as well as coal mine dust, can stimulate the release of monocyte-/macrophagederived proinflammatory cytokines, such as tumour necrosis factor (TNF)-α [3][4][5], interleukin-1β (IL-1β) [4,6,7], interleukin-6 (IL-6) [5], and the macrophage inflammatory proteins la and 2 [8]. With regard to dust exposure in man, we found that monocyte TNF release upon ex-vivo stimulation with coal dust and silica (and endotoxin) was increased in (retired) miners with or without radiological evidence for simple coal workers pneumoconiosis (CWP) compared to subjects never exposed to mineral dust [3,9].…”

mentioning

confidence: 99%

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Plasma levels of soluble tumour necrosis factor receptors are increased in coal miners with pneumoconiosis

Schins¹,

Borm²

1995

Eur Respir J

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P Pl la as sm ma a l le ev ve el ls s o of f s so ol lu ub bl le e t tu um mo ou ur r n ne ec cr ro os si is s f fa ac ct to or r r re ec ce ep pt to or rs s a ar re e i in nc cr re ea as se ed d i in n c co oa al l m mi in ne er rs s w wi it th h p pn ne eu um mo oc co on ni io os si is s ABSTRACT: Among other cytokines, tumour necrosis factor (TNF)-α is considered to play a key role in the development of mineral dust related fibrosis. Previously, we showed that ex-vivo release of TNF by peripheral blood monocytes is a marker for progression of coal workers' pneumoconiosis (CWP). Since soluble TNF receptors (sTNF-Rs) are believed to play an important regulatory role in systemic effects of TNF, we measured plasma levels of sTNF-R55 and sTNF-R75 in coal miners with (n=28) or without (n=76) CWP and in nonexposed controls (n=29).sTNF-R75 levels were significantly increased in miners with CWP (2.09±0.44 ng·mL -1 ) versus the nonexposed controls (1.86±0.23 ng·mL -1 ). Neither sTNF-R55 nor sTNF-R75 were related to exposure, stage of pneumoconiosis, smoking, or (spontaneous or ex-vivo induced) monocyte TNF-release. sTNF-R55 was increased in subjects with medication (especially those using cardiovascular drugs); upon exclusion of these subjects, sTNF-R55 was found also to be significantly increased in CWP.In conclusion, bearing in mind a confounding effect of medication, soluble TNF receptors are elevated in plasma of retired miners with coal workers' pneumoconiosis. These observations further support the important role of TNF-mediated pathways in the pathogenesis of mineral dust related fibrosis.

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confidence: 80%

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confidence: 99%

Plasma levels of soluble tumour necrosis factor receptors are increased in coal miners with pneumoconiosis

Schins¹,

Borm²

1995

Eur Respir J

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“…Enhanced levels of interferon-gamma (IFN-γ), IL-12p40 messenger ribonucleic acid (mRNA) and proteins have been observed in an experimental model of silicosis, suggesting that a T-helper (Th)-1 lymphocyte subpopulation might dominate in this disease. Several studies supported the view that the inflammatory and fibrotic responses of the lungs to crystalline silica are mediated by proinflammatory macrophage cytokines [3,14,[19][20][21][22]. The activated macrophages produce TNFalpha, interleukin-1 (IL-1), interleukin-6, leukotriene B4 (LTB4) and take part as а trigger for the developing pulmonary fibrosis [13].…”

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confidence: 99%

Serum neopterin in workers exposed to inorganic dust containing free crystalline silicon dioxide

et al. 2009

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AbstractThe study was conducted among 92 male workers, divided into two groups depending on workplace and level of inorganic dust containing free crystalline SiO2 in the work environment, and 43 healthy workers without exposure to dust aerosols. The measured inhalable and respirable dust concentrations, as well as the concentration of free crystalline silica (FCS) in the respirable fraction were different for the two groups, but the percentage of free crystalline silica in the respirable fraction was almost identical. Significantly higher neopterin levels were found in workers exposed to dust, compared to the control group: 12.72 nmol/L and 6.32 nmol/L respectively (p<0.05). No significant difference was found between serum neopterin levels in both groups of the exposed workers. Among the groups with different length of service, a statistically higher neopterin level was evident only in the workers with length of service less than 10 years (p<0.05). The correlation analysis did not find a significant dependence of neopterin levels on the age of the studied workers or on the duration of smoking in packet years. The difference between neopterin levels in smokers and non-smokers was nonsignificant. The results obtained show that increased neopterin levels in the exposed workers are not influenced by individual features, duration and level of exposure to inorganic dust, but mostly by the presence of FCS in the respirable fraction.

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“…These inflammatory mediators also play a role in the remodelling process through stimulation of fibroblast proliferation and collagen synthesis [2,3]. Increased levels of tumour necrosis factor (TNF)-a, interleukin (IL)-1, IL-6 and intercellular cell adhesion molecule (ICAM)-1 have been found in experimental models of pulmonary fibrosis [4,5] and in the airways of coal miners [6,7]. Continuous release of TNF-a from alveolar macrophages has been reported in miners with PMF [7].…”

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confidence: 99%

Genetic susceptibility to progressive massive fibrosis in coal miners

Yücesoy¹,

Johnson²,

Kissling³

et al. 2008

European Respiratory Journal

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Progressive massive fibrosis (PMF) is a chronic interstitial lung disease with a complex aetiology that can occur after cumulative dust exposure. A case-control study was conducted to test the hypothesis that single nucleotide polymorphisms (SNPs) within genes involved in inflammatory and fibrotic processes modulate the risk of PMF development.The study population consisted of 648 underground coal miners participating in the National Coal Workers Autopsy Study, of which 304 were diagnosed with PMF. SNPs that influence the regulation of interleukin (IL)-1, IL-6, tumour necrosis factor-a, transforming growth factor-b1, vascular endothelial growth factor (VEGF), epidermal growth factor intercellular cell adhesion molecule (ICAM)-1 and matrix metalloproteinase-2 genes were determined using a 59-nuclease real-time PCR assay.There were no significant differences in the distribution of any individual SNP or haplotype between the PMF and control groups. However, the polygenotype of VEGF +405/ICAM-1 +241/IL-6 -174 (C-A-G) conferred an increased risk for PMF (odds ratio 3.4, 95% confidence interval 1.3-8.8).The present study suggests that the examined genetic variations that help regulate inflammatory and fibrotic processes are unlikely to strongly influence susceptibility to this interstitial lung disease, although the role of vascular endothelial growth factor, intercellular cell adhesion molecule-1 and interleukin-6 polymorphisms in the development of progressive massive fibrosis may require further investigation.

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Abnormal Secretion of Interleukin-1 and Tumor Necrosis Factor α by Alveolar Macrophages in Coal Worker's Pneumoconiosis: Comparison between Simple Pneumoconiosis and Progressive Massive Fibrosis

Cited by 69 publications

References 7 publications

Plasma levels of soluble tumour necrosis factor receptors are increased in coal miners with pneumoconiosis

Plasma levels of soluble tumour necrosis factor receptors are increased in coal miners with pneumoconiosis

Serum neopterin in workers exposed to inorganic dust containing free crystalline silicon dioxide

Genetic susceptibility to progressive massive fibrosis in coal miners

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