title: Repair of astrocytes, blood vessels, and myelin in the injured brain: possible roles of blood monocytes.
abstract: Inflammation in injured tissue has both repair functions and cytotoxic consequences. However, the issue of whether brain inflammation has a repair function has received little attention. Previously, we demonstrated monocyte infiltration and death of neurons and resident microglia in LPS-injected brains (Glia. 2007. 55:1577; Glia. 2008. 56:1039). Here, we found that astrocytes, oligodendrocytes, myelin, and endothelial cells disappeared in the damage core within 1-3 d and then re-appeared at 7-14 d, providing evidence of repair of the brain microenvironment. Since round Iba-1+/CD45+ monocytes infiltrated before the repair, we examined whether these cells were involved in the repair process. Analysis of mRNA expression profiles showed significant upregulation of repair/resolution-related genes, whereas proinflammatory-related genes were barely detectable at 3 d, a time when monocytes filled injury sites. Moreover, Iba-1+/CD45+ cells highly expressed phagocytic activity markers (e.g., the mannose receptors, CD68 and LAMP2), but not proinflammatory mediators (e.g., iNOS and IL1β). In addition, the distribution of round Iba-1+/CD45+ cells was spatially and temporally correlated with astrocyte recovery. We further found that monocytes in culture attracted astrocytes by releasing soluble factor(s). Together, these results suggest that brain inflammation mediated by monocytes functions to repair the microenvironment of the injured brain.
authors.affiliation: Neuroscience Graduate Program, Department of Biomedical Sciences, Ajou University School of Medicine, Suwon, Kyunggi-do 443-721, Korea.
authors.forename: Hey-Kyeong
authors.initials: HK
authors.lastname: Jeong
authors.forename: Kyung-Min
authors.initials: KM
authors.lastname: Ji
authors.forename: Jun
authors.initials: J
authors.lastname: Kim
authors.forename: Ilo
authors.initials: I
authors.lastname: Jou
authors.forename: Eun-Hye
authors.initials: EH
authors.lastname: Joe
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000473:pathology*; D001808:Blood Vessels / Q000187:drug effects / Q000473:pathology*; D001930:Brain Injuries / Q000097:blood* / Q000473:pathology* / Q000503:physiopathology; D002465:Cell Movement / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D042783:Endothelial Cells / Q000187:drug effects / Q000473:pathology; D007249:Inflammation / Q000473:pathology; D019394:Ki-67 Antigen / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D009186:Myelin Sheath / Q000378:metabolism*; D016501:Neurites / Q000187:drug effects / Q000473:pathology; D020411:Oligonucleotide Array Sequence Analysis; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000187:drug effects; D013378:Substantia Nigra / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D014945:Wound Healing / Q000187:drug effects
chemical_list: D019394:Ki-67 Antigen; D008070:Lipopolysaccharides; D012333:RNA, Messenger