Accession Number:

ADA508692

Title:

The Role of Microglial Subsets in Regulating Brain Injury

Descriptive Note:

Annual rept. 1 Jul 2008-30 Jun 2009

Corporate Author:

NORTHERN CALIFORNIA INST FOR RESEARCH AND EDUCATION SAN FRANCISCO

Personal Author(s):

Report Date:

2009-07-01

Pagination or Media Count:

24.0

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 macrophagemicroglia 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.

Subject Categories:

  • Anatomy and Physiology
  • Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE