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Published on: November 23, 2014
Changes in phagocytosis and expression of microglial cells in craniocerebral injury mice models
1Department of Traumatic Surgery, Tongji Hospital, Tongji Medical College of Huazhong, University of Science and Technology, Wuhan, PR China.
Abstract:
The objective of this study was to investigate the changes in phagocytic function and expression quantities of CD11b and tumor necrosis factor-α (TNF-α) among microglia cells of craniocerebral injury mice. Modified Feeney method was used to establish the craniocerebral injury mice models. Twenty-one male SPF mice were divided into a control group and a trauma group. The scalp was incised and a bone window was opened in the control group without cerebral injury. In the trauma group, the mice were sacrificed after the craniocerebral injury at 1, 3, 6, 12, 24 and 48 h to make frozen sections of cerebral tissues. The phagocytic rate of microglia cells was observed by using fluorescent microsphere. The changes in the expression quantities of CD11b and TNF-α were detected by enzyme-linked immuno sorbent assay (ELISA). The phagocytic ability of the microglia cells after the craniocerebral injury increased at 1 h after injury compared with that of the control group (P less than 0.01). The expression of surface antigen CD11b of the microglia cells and the expression of TNF-α increased at 1, 3, 6, 12, 24 and 48 h after the injury compared with those of the control group (P less than 0.01). The phagocytic ability of the microglia cells increased. The expressions of CD11b and TNF-α were also gradually enhanced in the acute phase after craniocerebral injury, and then gradually decreased to the normal level. The expressions of CD11b and TNF-α indicated a high consistency with the changing trend of the phagocytic ability, suggesting that the microglia cells may participate in the regulation of the inflammatory process of the central nervous system through absorbing apoptotic cells and increasing and secreting inflammatory and anti-inflammatory factors.
Insights
Microglia cells in craniocerebral injury mice show increased phagocytic function and expression of CD11b and tumor necrosis factor-α (TNF-α). These changes correlate with the inflammatory response, suggesting microglia
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Craniocerebral injury triggers complex cellular responses in the central nervous system.
- Microglia are the primary immune cells in the brain and play a critical role in neuroinflammation.
Purpose of the Study:
- To investigate alterations in microglia phagocytic function following craniocerebral injury.
- To examine the expression levels of CD11b and tumor necrosis factor-α (TNF-α) in microglia post-injury.
Main Methods:
- Establishment of craniocerebral injury mouse models using a modified Feeney method.
- Assessment of microglia phagocytic rate using fluorescent microspheres.
- Quantification of CD11b and TNF-α expression via enzyme-linked immunosorbent assay (ELISA).
Main Results:
- Microglia phagocytic ability significantly increased at 1 hour post-injury.
- Expression of CD11b and TNF-α were elevated from 1 to 48 hours after injury.
- Phagocytic ability and CD11b/TNF-α expression showed a high degree of correlation.
Conclusions:
- Microglia exhibit enhanced phagocytic activity and increased CD11b and TNF-α expression in the acute phase after craniocerebral injury.
- These findings suggest microglia actively participate in the central nervous system's inflammatory response by engulfing apoptotic cells and modulating inflammatory factors.
