title: Substance P induces M2-type macrophages after spinal cord injury.
abstract: The potential benefits or the tissue-damaging effects of inflammatory response after central nervous system injuries have long been disputed. Recent studies have noted that substance P (SP), a neuropeptide, plays an important role in the wound-healing process by recruiting bone marrow stem cells to the injured tissue. In this study, we examined whether SP can enhance recovery from spinal cord injury (SCI) in Sprague-Dawley rats through its known function of stem cell mobilization and/or through the modulation of inflammation. We examined proinflammatory and anti-inflammatory cytokines and markers for macrophage subtypes. SP treatment modulated the SCI microenvironment toward a more anti-inflammatory and reparative one by inducing interleukin-10 and M2 macrophages and suppressing inducible nitric oxide synthase and tumor necrosis factor-α. This modulation was achieved at 1 day much earlier than SP-stimulated bone marrow stem cells' mobilization. Early intervention of the devastating inflammatory response by SP treatment caused the lesion cavity to become filled with robust axonal outgrowth that overlaid the M2 macrophages at 2 weeks--all of which culminated in tissue sparing and improvement in functional recovery from the SCI. SP is therefore a potential anti-inflammatory modulator for the treatment of injury-induced inflammatory central nervous system disorders.
authors: Department of Genetic Engineering, College of Life Science and Graduate School of Biotechnology, Kyung Hee University, Yong In, Korea.
authors: Mei H
authors: MH
authors: Jiang
authors: Eunkyung
authors: E
authors: Chung
authors: Guang F
authors: GF
authors: Chi
authors: Woosung
authors: W
authors: Ahn
authors: Ji E
authors: JE
authors: Lim
authors: Hyun S
authors: HS
authors: Hong
authors: Dae W
authors: DW
authors: Kim
authors: Hyeongwon
authors: H
authors: Choi
authors: Jiyoung
authors: J
authors: Kim
authors: Youngsook
authors: Y
authors: Son
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001369:Axons / Q000187:drug effects* / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy; D016753:Interleukin-10 / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects*; D008297:Male; D017628:Microglia / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000187:drug effects; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013373:Substance P / Q000378:metabolism / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D013373:Substance P