Single Intratracheal Quartz Instillation Induced Chronic Inflammation and Tumourigenesis in Rat Lungs

Abstract

crystalline silica (quartz) is known to induce silicosis and cancer in the lungs. in the present study, we investigated the relationship between quartz-induced chronic inflammation and lung carcinogenesis in rat lungs after a single exposure to quartz. F344 rats were treated with a single intratracheal instillation (i.t.) of quartz (4 mg/rat), and control rats were treated with a single i.t. of saline. After 52 or 96 weeks, the animals were sacrificed, and the lungs and other organs were used for analyses. Quartz particles were observed in the lungs of all quartz-treated rats. According to our scoring system, the lungs of rats treated with quartz had higher scores for infiltration of lymphocytes, macrophages and neutrophils, oedema, fibrosis, and granuloma than the lungs of control rats. After 96 weeks, the quartz-treated rats had higher incidences of adenoma (85.7%) and adenocarcinoma (81.0%) than control rats (20% and 20%, respectively). Quartz-treated and control rats did not show lung neoplastic lesions at 52 weeks after treatment. The number of lung neoplastic lesions per rat positively correlated with the degree of macrophage and lymphocyte infiltration, oedema, fibrosis, and lymph follicle formation around the bronchioles. In conclusion, single i.t. of quartz may induce lung cancer in rat along with chronic inflammation.

Dynamic assessing silica particle-induced pulmonary fibrosis and associated regulation of long non-coding RNA expression in Wistar rats

“…We observed significant changes in body weight of rats in the silica-exposed group on day 28 ( P ≤ 0.05) and the lung coefficient silica-exposed rats were significantly increased when compared to controls on day 28 ( P < 0.01) [ 22 ]. In animal models, both accelerated silicosis with high-dose silica and chronic silicosis with low-dose silica exposures induce granulomatous changes in the lung [ 30 , 31 ]. The granuloma-like structures in accelerated silicosis are loosely aggregated foamy histiocytes [ 32 ].…”

“…Lung inflammation and apoptosis are hallmarks of accelerated silicosis. However, diffusibility granulomas arise by chronic inhalation of silica without significant lung inflammation or apoptosis [ 31 ]. In our study, the inflammatory cells appeared from the first day and increased until day 14.…”

Inhibitory Effects of Breast Milk-Derived Lactobacillus rhamnosus Probio-M9 on Colitis-Associated Carcinogenesis by Restoration of the Gut Microbiota in a Mouse Model

“…Mouse tissue specimens were immunostained by the labeled streptavidin-biotin method using the Ventana Discovery staining system (Ventana Medical Systems, Oro Valley, AZ, USA) with DISCOVERY DAB Map Detection Kit (Roche, Basel, Switzerland). The anti-mouse CD3 monoclonal antibody (1:150 dilution); the anti-mouse CD68 polyclonal antibody (1:100 dilution), anti-mouse CD163 monoclonal antibody (1:500 dilution), and anti-mouse Ki-67 and PCNA monoclonal antibodies (1:200 dilution) used were diluted with DISCOVERY Antibody Diluent (Roche, Switzerland) [21]. For CD163 samples, cell conditioning 1 (CC1, pH 8.5, Roche) antigen activation was performed for 60 min at 100 • C. For other samples, RiboCC (pH 6.0, Roche, Switzerland) antigen activation was performed for 60 min at 100 • C. The reaction times of the primary antibody were CD3, 60 min and the others, 12 h. The reaction time of the second antibody were CD3, 60 min and the others, 32 min.…”

Relationship between Lung Carcinogenesis and Chronic Inflammation in Rodents

“…Interstitial pneumonia, a condition that causes progressive fibrosis, is a known risk factor for lung carcinogenesis independent of smoking; epidemiologically, the risk of lung carcinogenesis is 6.42 times in healthy subjects [5]. Silicosis is induced by chronic occupational exposure to quartz [7]. A significant positive relationship between cumulative silica exposure and lung cancer mortality has already been reported [119]; in this study, 1079 of 65,980 silica-exposed workers died due to lung cancer.…”

“…Other than tobacco, there are various risk factors, such as radon, inhalation of fine or nano particles (e.g., asbestos, clistalin silica, etc. ), domestic fuel smoke (biomass), e-cigarettes, occupational hazards, air pollution, sex, steroids, infectious diseases, interstitial pneumonia (especially idiopathic pulmonary fibrosis), previous radiation therapy of the lungs and family history of lung cancer [4][5][6][7][8]. Although genetic mutations underlie malignant transformation, the presence of mutations alone is not sufficient for tumor formation, and additional alterations are necessary for the development of cancer [9,10].…”