Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037116 (silicosis)
 1,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Excessive exposure to respirable particles of crystalline silica is an occupational health problem in developing countries and can cause a variety of pulmonary diseases, such as silicosis, chronic obstructive pulmonary disease (COPD), and malignancy, in susceptible hosts. In addition to the well-documented role of pulmonary macrophages, lymphocytes occasionally have been suggested to influence the pneumoconiotic process, but their potential role is not clearly understood. Interferon-gamma (IFN-gamma), a lymphocyte cytokine, is recognized as the most important cytokine in converting macrophages from a resting to an activated state. The aim of the present study was to investigate serum IFN-gamma levels and pulmonary function changes in silica-exposed workers and in silicosis. Twenty-seven silica workers (aged 35.6 +/- 8.2 years with 5.11 +/- 2.98 years exposure duration) and 18 unexposed office workers (aged 33.8 +/- 12 years) were included in the study. Mean spirometry parameters and smoking history were comparable to the values of the office workers, but COPD prevalence was higher in the silica-exposed group, and the age-adjusted ratio was more sensitive than fixed quotient criteria for airway obstruction. We found silicosis in 4 silica workers. The mean serum IFN-gamma level was increased in silica-exposed workers (10.22 +/- 22.68 pg/mL) although it was undetectable in all office workers and even in the workers with silicosis. Evaluating pulmonary function tests (PFT) using an age-adjusted quotient may prevent underestimation of airflow limitation, especially in the young population with risk factors. Although serum IFN-gamma may increase initially in response to silica, low levels of IFN-gamma in later stages may be considered a risk factor for silicosis because this cytokine downregulates the fibroblast responses to transforming growth factor-beta (TGF-beta) and decreases collagen production. Additional research to determine the exact role of this potent cytokine may offer insight into the pathogenesis of silicosis.
J Interferon Cytokine Res 2008 May
PMID:Lung function and IFN-gamma levels in the sera of silica-exposed workers. 1854 61

This study aimed to assess the association of Tumor Necrosis Factor (TNF-alpha) Locus-308 variant, TNF-alpha and Interleukin (IL-10) Cytokine with the risk of silicosis and its progress in Indonesian cement factory workers, There is an urgent need to explore the determining factors other than exposure since silicosis is chronic progressive and life threatening but remains found, though much industrial hygiene effort has been made. This study population was 6,069 workers registered during 31 December 1990 to 31 December 2003. First, prospective study with Nested Case Control design was conducted on 336 workers in 2003, ten years later the progression of silicosis was assessed in 2013. The result showed proportion of the genetic variation on TNF-alpha on Locus -308 in Indonesia was significantly (p = 0.02) higher on silicosis (13.45%) than nonsilicosis (5.45%) but lower than silicosis in Africa and US miners, since susceptibility loci might vary in different ethnic groups. The sign and symptoms remained as simple silicosis after ten years; The TNF-alpha:IL-10 ratio > 1 was a risk factor in silicosis; the ratio of TNF-alpha:IL-10 > 1 caused a rapid decline of lung function compare to ratio < 1, the decline was chronic progressive during ten years yet not causing significant dyspnea among the cases. Further studies with enlarged sample size are needed. The study concluded, the genetic variation on TNF-alpha gene locus -308 was a risk factor of silicosis in Indonesia cement factory. Its role is indirect, but through mechanism of controlling the blood Cytokine level ratio of TNF-alpha toward IL-10.
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PMID:Silicosis and its progress influenced by genetic variation on TNF-alpha locus- 308, TNF-alpha and IL-10 cytokine on cement factory workers in Indonesia. 2489 98

Silicosis is a long-established public health issue in developing countries due to increasingly serious air pollution and poorly implemented occupational safety regulation. Inhalation of silica triggers cytotoxicity, oxidative stress, pulmonary inflammation and eventually silicosis. Current understanding in the pathogenesis and mechanism of silicosis is limited, and no effective cure is clinically available once silicosis is developed. A number of studies were conducted to investigate silica-induced alternate gene expressions in pulmonary cells. However, transcriptome analysis in a silicosis animal model is needed. This study was performed to evaluate the transcriptional alternations in silicotic mice using comparative RNA-Seq. A silicosis mice model was established by intratracheal instillation of silica suspensions, and validated by histological examinations. High-throughput sequencing and differential gene expression analysis revealed 749 upregulated genes and 70 downregulated genes in the silicosis model. Genes related to immune cell interactions, immune cell responses and inflammation were significantly enriched. Cytokine-cytokine receptor interaction and downstream JAK-STAT signaling pathways were the most significantly enriched KEGG pathways. Reverse transcription-polymerase chain reaction analysis and immunohistochemistry were performed to validate further the differential expression patterns of representative genes. The reported results in this study provide the basis for elucidating the molecular mechanisms for silica-induced pulmonary inflammation and fibrosis, and support the prevention and treatment of silicosis.
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PMID:Comparative RNA-Seq transcriptome analysis on silica induced pulmonary inflammation and fibrosis in mice silicosis model. 2934 Dec 24