Pathological comparison of lipopolysaccharide- and graphite particle-induced acute lung injury
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    Abstract:

    Objective To compare the differences of lung pathological changes of acute lung injury in mice induced by lipopolysaccharide (LPS) and graphite particles, and to explore the possible mechanisms of acute lung injury induced by fine particles of different origins. Methods 140 male specific-pathogen-free Kunming mice weighing 18-20 g were randomly divided into 7 experimental groups, in addition to the normal control group. The experimental groups were treated by intratracheal instillation of LPS solution or graphite powder suspension in different doses, respectively, to induce acute lung injury in the mice. The mortality of the mice was observed, and pathological changes of the lung tissues were examined by light and transmission electron microscopy. Western blot was used to detect the protein expression of neutrophil elastase (NE) in lung tissues , and real-time quantitative PCR was used to detect mRNA expression of monocyte chemotactic protein-1 (MCP-1)in the lung tissue . Results Compared with the normal control group, some pathological changes were observed in the lung tissues of the groups L (LPS) and G (graphite). There were numerous macrophages in the lung tissues in the group G mice, and exudate, mainly neutrophils, in the lung tissues of the group L. The NE protein expression in the lung tissue was significantly higher than that of the normal control group (P<0.05), and there was also a significant difference between the groups L and G (P<0.05). The MCP-1 mRNA expression in lung tissues was higher in the control group (P<0.01), and there was also a significant difference between the groups L and G (P<0.01). Conclusions Diverse types of particulate matters induce different pathological changes in the lungs, therefore the mechanism may also be different in the inflammatory responses. It means that the lung injuries caused by fine particles of mixed composition may have complex mechanisms.

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  • Received:May 19,2014
  • Online: October 30,2014
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