Abstract
BackgroundAlthough nitric oxide is overproduced by macrophages and neutrophils after exposure to silica, its role in silica-induced inflammatory reaction and apoptosis needs further clarification. In this study, rats were intratracheally instilled with either silica suspension or saline to examine inflammatory reactions and intraperitoneally injected with ω-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthases, or saline to examine the possible role of nitric oxide production in the reaction.ResultsResults showed that silica instillation induced a strong inflammatory reaction indicated by increased total cell number, number of neutrophils, protein concentration and lactate dehydrogenase (LDH) activity in bronchoalveolar lavage fluid (BALF). There were no significant differences in these indices between silica-instilled groups with and without L-NAME injection (p > 0.05) except LDH level. The results also showed that apoptotic leucocytes were identified in BALF cells of silica-instilled groups whereas no significant difference was found between silica-instilled groups with and without L-NAME injection in the apoptotic reaction (p > 0.05). Silica instillation significantly increased the level of BALF nitrite/nitrate and L-NAME injection reduced this increase.ConclusionIntratracheal instillation of silica caused an obvious inflammatory reaction and leucocyte apoptosis, but these reactions were not influenced by intraperitoneal injection of L-NAME and reduced production of NO. This supports the possibility that silica-induced lung inflammation and BALF cell apoptosis are via NO-independent mechanisms.
Highlights
Nitric oxide is overproduced by macrophages and neutrophils after exposure to silica, its role in silica-induced inflammatory reaction and apoptosis needs further clarification
There was no significant difference in total cell number of bronchoalveolar lavage fluid (BALF) between silica + saline and silica + L-NAME groups (p > 0.05, Figure 1)
The protein concentration in BALF of silica-instilled groups significantly (p < 0.05) increased compared with saline-instilled groups but no significant difference could be detected between the silica-instilled groups with and without L-NAME injection (Figure 4)
Summary
Nitric oxide is overproduced by macrophages and neutrophils after exposure to silica, its role in silica-induced inflammatory reaction and apoptosis needs further clarification. Silica exposure results in an initial inflammatory reaction and subsequent fibrosis During this process, various agents such as cytokines and free radicals are produced and these agents in turn regulate the development of the inflammation and fibrosis [1]. Nitric oxide (NO), a small molecule with multiple biologic functions, has been shown to be overproduced by alveolar macrophages and neutrophils as well as other cell types after exposure to intratracheal instillation of silica [2,3,4]. NO is a molecule that can readily pass through the cell membrane and exert its action on cells It is involved in vessel dilatation, inhibition of platelet aggregation [7] and host defence. It is an apoptosis inducer for some cell (page number not for citation purposes)
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