Immunogenetic sudies on HLA-DR in German coal miners with and without coal worker's pneumoconiosis

Hp, Rihs; Lipps, P; May-Taube, K; Jäger, D; Ew, Schmidt; Jh, Hegemann; Baur, Xaver

doi:10.1007/bf00172848

Cited by 14 publications

(8 citation statements)

References 21 publications

(31 reference statements)

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“…Several studies have been reported in coal workers with CWP, but no studies in coal workers are available linking allelic polymorphs to TNF release. In German coal workers, the frequency of DR8 was elevated in miners with CWP, whereas the frequency of DR1 and DR52 was reduced in miners without CWP [Rihs et al, 1994]. Studies among Japanese subjects with silicosis indicated that HLA Ϫ B54 Ϫ DR4 Ϫ DR53 are positive and HLA Ϫ B52 Ϫ DR4 Ϫ DR2 negative linkage disequilibrium with silicosis respectively [Honda et al, 1993].…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms in the promoter of the tumor necrosis factor-? gene in coal miners

et al. 1998

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Tumor necrosis factor‐α (TNF) is recognized as a central mediator of mineral dust‐induced lung fibrosis, and genetic polymorphisms of the TNF promoter have been reported to influence levels of TNF production. To assess whether polymorphisms within the TNF promoter gene are associated with susceptibility to coal workers' pneumoconiosis (CWP), the DNA of 78 coal miners was typed for G‐to‐A transitions at positions −238 and −308. Our results show that frequency of A−308 genotype (T2) is significantly overpresented in coal miners with CWP (50%), as compared with miners without CWP (25%) and controls (29%). After correction for cumulative dust exposure and smoking, the A−308 transition genotype is still associated with the presence of CWP (OR = 3.0, 95%CI = 1.0–9.0). Both A−238 and A−308 transition genotypes were related to TNF release from endotoxin‐stimulated blood monocytes; only the A−238 transition and not the A−308 transition was associated to coal dust‐induced TNF release. In summary, this study shows that the A−308 transition is related to CWP, but this relation is not paralleled by a different TNF release in this genotype. A larger number of patients coupled to frequent TNF release are required to evaluate genotype screening to estimate individual health risks for effects of coal mine dust exposure. Am. J. Ind. Med. 34:318–324, 1998. © 1998 Wiley‐Liss, Inc.

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Section: Discussionmentioning

confidence: 99%

Polymorphisms in the promoter of the tumor necrosis factor-? gene in coal miners

et al. 1998

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“…The severity of these diseases is related to the total dose and intensity of dust exposure. However, inter-individual differences in lung responses to the same amount of dust exposure have been described which suggest a genetic influence on the host defense to environmental exposure [Eden and Seebach, 1976;Katsnelson et al, 1986;Rihs et al, 1994;Ohtsuka et al, 1995;Davis et al, 1998a;Kim et al, 2002]. Progressive massive fibrosis (PMF), a conglomeration of small rounded opacities, is one of the major risks of mortality in patients with CWP [Lassalle et al, 1990].…”

Section: Introductionmentioning

confidence: 98%

Antithetical effect of tumor necrosis factor-αgene polymorphism on coal workers' pneumoconiosis (CWP)

et al. 2005

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“…Associations of specific human leukocyte antigen (HLA) haplotype with silicosis have been reported in a Japanese population [3]. In a German population, HLA haplotype association with coal worker's pneumoconiosis has also been reported [4]. Associations of gene polymorphisms of pro-inflammatory cytokines (e.g.…”

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Genetic linkage analysis of pulmonary fibrotic response to silica in mice

Ohtsuka¹,

Xt²,

Saito³

et al. 2006

European Respiratory Journal

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Inter-individual variations in the development of silicosis, even within the same environments, have been reported, which suggest the contribution of genetic factors in silicosis aetiology. The aim of the present study was to determine whether there is any significant genetic influence on the development of silicosis. Furthermore, which genetic loci are responsible for the pulmonary response to silica exposure?Eight strains of inbred mice were used to examine the genetic influence on the lung fibrotic response to silica exposure. After intercross-breeding between the most susceptible and most resistant strains, a genome-wide linkage analysis of quantitative trait loci (QTL) was performed. Hydroxyproline was applied as an index, and genotypes of 167 marker genes were analysed by fragment analysis using a capillary-type sequencer.There was significant inter-strain difference in the mean concentration of hydroxyproline contents among the eight strains of mice. Breeding studies were conducted between the most susceptible, C57BL/6J, and the most resistant strain, CBA/J. A genome-wide linkage analysis of silica-exposed intercrossed cohorts identified significant QTL on chromosome 4 and suggestive QTL on chromosomes 3 and 18.The present study demonstrates that genetic factors may play a significant role in fibrotic-lung responses to silica; one significant and two suggestive quantitative trait loci were identified.

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Immunogenetic sudies on HLA-DR in German coal miners with and without coal worker's pneumoconiosis

Cited by 14 publications

References 21 publications

Polymorphisms in the promoter of the tumor necrosis factor-? gene in coal miners

Polymorphisms in the promoter of the tumor necrosis factor-? gene in coal miners

Antithetical effect of tumor necrosis factor-αgene polymorphism on coal workers' pneumoconiosis (CWP)

Genetic linkage analysis of pulmonary fibrotic response to silica in mice

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