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.
There is evidence showing a crucial role for tumor necrosis factor-a (TNF-alpha) and interleukin-1 (IL-1) in inflammation caused by silica dust and in the transition from simple to progressive massive fibrosis.
The number of positive cells found in BALF was significantly higher for patients with PMF (TNF = 55 +/- 6%; IL-6 = 46 +/- 12.8%) than for those with SP (TNF = 34 +/- 11.6%; IL-6 = 26 +/- 10.2%) or normal controls (TNF = 15 +/- 5.5%; IL-6 = 13.3 +/- 6%), and was correlated with cytokine concentrations in supernatants from alveolar macrophages (AM).
The number of positive cells found in BALF was significantly higher for patients with PMF (TNF = 55 +/- 6%; IL-6 = 46 +/- 12.8%) than for those with SP (TNF = 34 +/- 11.6%; IL-6 = 26 +/- 10.2%) or normal controls (TNF = 15 +/- 5.5%; IL-6 = 13.3 +/- 6%), and was correlated with cytokine concentrations in supernatants from alveolar macrophages (AM).
The proportion of federal black lung benefits claimants with PMF has been increasing since 1978 (0.06% annual percent change [APC]; 95% confidence interval [CI], 0.05-0.07%; P < 0.0001), and began increasing at a significantly increased rate after 1996 (0.26% APC; 95% CI, 0.25-0.28%; P < 0.0001).
MBL2 polymorphisms (codon54, promoter -221, and -550) were assessed for 197 patients with CWP (119 with nodular CWP and 78 with PMF) and 153 unexposed regional controls.
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.
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).
However, by assessing duration of work and its interaction with genotypes by means of logistic regression, the authors found the missense C/T polymorphism in exon 6 of the PLAU gene to be an effect modifier of the association between work duration and the development of progressive massive fibrosis.
A matched case-control study was conducted to determine the influence of the GSTP1, GSTT1 and MnSOD polymorphisms on susceptibility to progressive massive fibrosis (PMF).
A matched case-control study was conducted to determine the influence of the GSTP1, GSTT1 and MnSOD polymorphisms on susceptibility to progressive massive fibrosis (PMF).
There is evidence showing a crucial role for tumor necrosis factor-a (TNF-alpha) and interleukin-1 (IL-1) in inflammation caused by silica dust and in the transition from simple to progressive massive fibrosis.
There is evidence showing a crucial role for tumor necrosis factor-a (TNF-alpha) and interleukin-1 (IL-1) in inflammation caused by silica dust and in the transition from simple to progressive massive fibrosis.