The Role of Microglial Subsets in Regulating Brain Injury
Abstract
Microglia are the innate immune cells of the brain. They share cell lineage with macrophages, which have been divided into two major subgroups: (i) classical or "M1" macrophages, which promote inflammation and express IL-12, and (ii) alternatively activated or "M2" macrophages, which phagocytose apoptotic cells, promote wound repair, and (in mice) express arginase-1. We proposed that microglia might be also reflect these functional subsets and that activation of microglia by TBI would be detrimental to the extent that it involves M1-like (pro-inflammatory) microglia, but beneficial to extent that it involves the activation of M2-like (reparative) microglia. To test this, we are studying TBI in "reporter" mice that express the fluor YFP under control of the promoter for either IL-12 or arginase-1. One day after TBI, we see little activation of microglia or macrophages. By day 4, ~20% of the combined macrophage/microglia population is activated, as assessed by marked enlargement. It is not yet clear whether these activated cells derive from macrophages or microglia. In this dramatic response, the enlarged cells have intrinsic fluorescence, requiring us to turn to additional means to fully characterize them, but our preliminary results indicate that they more readily express N-arginase than IL-12.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2009
- Accession Number
- ADA508692
Entities
People
- William E. Seaman
Organizations
- Northern California Institute for Research and Education