Disease relevance of Berylliosis

• Only one bFGF isoform (17.8 kd) was found in idiopathic pulmonary fibrosis and chronic beryllium disease lung tissues and interacted with heparin-like molecules in the lung [1].
• We hypothesized that alveolar macrophages and bronchoalveolar lavage fluid from patients with beryllium disease and sarcoidosis would express increased levels of mRNA and proteins, respectively, for TNF-alpha, IL-1 beta, and IL-6 compared with those of normal individuals [2].
• Comparison of a total of 1663 sequence tags in four berylliosis patients revealed a mean of 32.5-37.4% differentially regulated sequence tags in peripheral blood monocytes of berylliosis patients, caused by stimuli including beryllium or Mycobacterium tuberculosis and control stimuli such as Latex or Zymosan [3].

High impact information on Berylliosis

• HLA-DPB1 glutamate 69: a genetic marker of beryllium disease [4].
• Re: Lung cancer incidence among patients with beryllium disease [5].
• Influence of MHC class II in susceptibility to beryllium sensitization and chronic beryllium disease [6].
• Partial IL-10 inhibition of the cell-mediated immune response in chronic beryllium disease [7].
• Beryllium induces IL-2 and IFN-gamma in berylliosis [8].

Chemical compound and disease context of Berylliosis

• A glutamic acid at residue 69(Glu(69)) in the HLA-DPB1 gene (Glu(69)) is associated with chronic beryllium disease (CBD) and possibly beryllium sensitization (BeS) [6].
• Increased glutathione and glutathione peroxidase in lungs of individuals with chronic beryllium disease [9].
• Nitric oxide attenuates beryllium-induced IFNgamma responses in chronic beryllium disease: evidence for mechanisms independent of IL-18 [10].
• In seven patients with chronic beryllium disease (Be) the Be lymphocyte transformation test was positive in 100%, independent of steroid therapy, and was reproducible [11].
• Serum neopterin in chronic beryllium disease [12].

Gene context of Berylliosis

• In patients with beryllium disease (n = 23), we observed elevated macrophage mRNA expression for TNF-alpha and IL-6 when compared with that of normal subjects (n = 7) [2].
• We have tested the new method by genotyping the Glu69 variant from the HLA DPB1 locus, a SNP associated with chronic beryllium disease, as well as HLA DPA1 alleles using the multiplexed method [13].
• In vitro stimulation of bronchoalveolar lavage cells from patients with chronic beryllium disease (CBD) induces the production of TNF-alpha [14].
• We investigated the antioxidant response of the lungs to the chronic release of ROS, as occurs in the immune-specific granulomatous inflammation of chronic beryllium disease (CBD), and compared it with that in healthy controls and individuals exposed to cigarette smoke [9].
• Two gene markers have been previously associated with berylliosis: HLA-DP allelic variants carrying glutamate in position 69 of the beta-chain and the high TNF-alpha production-associated TNF-alpha promoter allele TNFA2 [15].

Analytical, diagnostic and therapeutic context of Berylliosis

• BACKGROUND: Several case-control studies have found an association between chronic beryllium disease (CBD) and HLA-DPB1 gene variants [16].

References