Relationship Between Mineral Fiber-Induced Pulmonary Tissue Reaction and MIP-2 / 대한산업의학회지

The pulmonary recruitment and activation of inflammatory cells, in particular, neutrophils is thought to contribute to lung injury resulting from dust exposure. MIP-2 (macrophage inflammatory protein-2) which is a member of C-X-C chemokine plays a key role in neutrophil recruitment to sites of tissue injury. Especially, mineral fiber induced pulmonary response is as a model for the neutrophil recruitment. Therefore, we evaluated the distribution of MIP-2 expression in lung tissue of mineral fiber exposed rat using immunohistochemical study and the relationship between degree of inflammation of lower respiratory tract and MIP-2 expression. Total cell counts in bronchoalveolar lavage (BAL) fluid in mineral fiber-exposed group were markedly increased compared with each control group even not in ceramic fiber group. Number of neutrophil in BAL fluid in mineral fiber-exposed group were markedly increased compared with each control group until 4th week but except ceramic fiber group. In chrysotile group, number of neutrophil in BAL fluid were markedly increased compared with control group at 8th week. Lung tissue instilled with all kinds of mineral fibers showed remarkable developments of bronchus associated lymphoid tissue (BALT) and small multiple granulomas but not for ceramic fiber group. In chrysotile group, multiple granuloma and inflammatory change were more profuse response compared with other groups. MIP-2 was predominently expresses in epithelial cells of bronchioles and bronchus and was express also found in macrophages with lung section at 1 week after fiber instillation. Small amount of epithelial cell associated MIP-2 was present in chrysotile at 8 week group. But MIP-2 was not seen in epithelial cells and macrophages in the lung tissue instilled with crocidolite, ceramic fiber and glass fiber at 8 weeks. Our finding suggest that MIP-2 is predominantly expressed in bronchial epithelial cells of lung from mineral fiber-exposed rat and correlated with inflammatory cell, especially neutrophil, recruitment and tissue reaction. And we documented that MIP-2 expression and neutrophil recruitment in man-made vitreous fiber-exposed rat, especially glass fiber, less than chrysotile.

Cytotoxicity and Apoptosis by Silica, Asbestos and Man-Made Mineral Fibers / 대한산업의학회지

Exposure to various particles and fibers can result in lung inflammation that may progress to fibrosis, even lung cancer for which there is no effective clinical treatment now. The mechanism involved in pulmonary injury has not been well defined ; however, most current evidence implicates a central role for alveolar macrophages (AM) in this process. Also apoptosis or programmed cell death is regarded as a mechanism which is related with the pulmonary fibrosis. We propose that the cytotoxic potential of various particles may be evaluated by measuring lactic dehydrogenase (LDH) from particle co-cultured supernatant and theses particles may induce the characteristics of apoptosis, DNA ladder. We analyzed rat AM culture media which was incubated for 3 days with the same concentration (10 ug/ml) of silica(Si), chrysotile(Ch), crocidolite(Cr), ceramic fiber(CF), rock wool(RW) and glass wool (GW). And each particles (50ug/cm(2)) was incubated with A549 (pneumocyte in tracheal epithelium) cell lines for 24 hours to confirm the DNA ladder. Additionally, silica induced apoptosis in vivo was confirmed by electromicroscopic observation. The results were as follows; 1. Silica, asbestos and man-made mineral fibers (MMMF) co-cultured with AM showed the increase of LDH significantly with the time interval of 24, 48, 72 hours except for ceramic fiber in 48 and 72 hours and crocidolite in 72 hours. 2. Silica, asbestos and man-made mineral fibers (CF, GF) showed the characteristics of apoptosis, DNA ladder, which was induced by incubating A549 cell with each particles for 24 hours in vitro 3. Apoptotic alveolar macrophage was observed the findings of zeiosis (membrane blebbing), condensation of nuclear chromosome and many vacuoles in cytoplasm, electomicroscopically.

Cytotoxicity and Apoptosis by Silica, Asbestos and Man-Made Mineral Fibers / 대한산업의학회지

Exposure to various particles and fibers can result in lung inflammation that may progress to fibrosis, even lung cancer for which there is no effective clinical treatment now. The mechanism involved in pulmonary injury has not been well defined ; however, most current evidence implicates a central role for alveolar macrophages (AM) in this process. Also apoptosis or programmed cell death is regarded as a mechanism which is related with the pulmonary fibrosis. We propose that the cytotoxic potential of various particles may be evaluated by measuring lactic dehydrogenase (LDH) from particle co-cultured supernatant and theses particles may induce the characteristics of apoptosis, DNA ladder. We analyzed rat AM culture media which was incubated for 3 days with the same concentration (10 ug/ml) of silica(Si), chrysotile(Ch), crocidolite(Cr), ceramic fiber(CF), rock wool(RW) and glass wool (GW). And each particles (50ug/cm(2)) was incubated with A549 (pneumocyte in tracheal epithelium) cell lines for 24 hours to confirm the DNA ladder. Additionally, silica induced apoptosis in vivo was confirmed by electromicroscopic observation. The results were as follows; 1. Silica, asbestos and man-made mineral fibers (MMMF) co-cultured with AM showed the increase of LDH significantly with the time interval of 24, 48, 72 hours except for ceramic fiber in 48 and 72 hours and crocidolite in 72 hours. 2. Silica, asbestos and man-made mineral fibers (CF, GF) showed the characteristics of apoptosis, DNA ladder, which was induced by incubating A549 cell with each particles for 24 hours in vitro 3. Apoptotic alveolar macrophage was observed the findings of zeiosis (membrane blebbing), condensation of nuclear chromosome and many vacuoles in cytoplasm, electomicroscopically.