muramidase and Hypoxia-Ischemia--Brain

Neonatal brain injury is increasingly understood to be linked to inflammatory processes that involve specialised CNS and peripheral immune interactions. However, the role of peripheral myeloid cells in neonatal hypoxic-ischemic (HI) brain injury remains to be fully investigated.. We employed the Lys-EGFP-ki mouse that allows enhanced green fluorescent protein (EGFP)-positive mature myeloid cells of peripheral origin to be easily identified in the CNS. Using both flow cytometry and confocal microscopy, we investigated the accumulation of total EGFP. We demonstrate a temporally biphasic pattern of inflammatory monocyte and granulocyte infiltration, characterised by peak infiltration at 1 day and 7 days after hypoxia-ischemia. This occurs against a backdrop of continuous low-level resident monocyte infiltration. Antibody-mediated depletion of circulating myeloid cells reduced immune cell accumulation in the brain and reduced neuronal loss in male but not female mice.. This study offers new insight into sex-dependent central-peripheral immune communication following neonatal brain injury and merits renewed interest in the roles of granulocytes and monocytes in lesion development.

Topics: Animals; Animals, Newborn; Antibodies; Antigens, Ly; Calcium-Binding Proteins; Cytokinins; Disease Models, Animal; Functional Laterality; Green Fluorescent Proteins; Hypoxia-Ischemia, Brain; Male; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microfilament Proteins; Monocytes; Muramidase; Myeloid Cells; Nerve Tissue Proteins; Neutrophils