Intracerebral complement C5a receptor (CD88) expression is regulated by TNF and lymphotoxin-α following closed head injury in mice

Philip F. Stahel*, Karin Kariya, Esther Shohami, Scott R. Barnum, Hans Pietro Eugster, Otmar Trentz, Thomas Kossmann, Maria C. Morganti-Kossmann

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

52 Scopus citations

Abstract

The anaphylatoxin C5a is a potent mediator of inflammation in the CNS. We analyzed the intracerebral expression of the C5a receptor (C5aR) in a model of closed head injury (CHI) in mice. Up-regulation of C5aR mRNA and protein expression was observed mainly on neurons in sham-operated and head- injured wild-type mice at 24 h. In contrast, in TNF/lymphotoxin-α knockout mice, the intracerebral C5aR expression remained at low constitutive levels after sham operation, whereas it strongly increased in response to trauma between 24 and 72 h. Interestingly, by 7 days after CHI, the intrathecal C5aR expression was clearly attenuated in the knockout animals. These data show that the posttraumatic neuronal expression of the C5aR is, at least in part, regulated by TNF and lymphotoxin-α at 7 days after trauma. (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)164-172
Number of pages9
JournalJournal of Neuroimmunology
Volume109
Issue number2
DOIs
StatePublished - 22 Sep 2000

Keywords

  • C5a
  • Complement
  • Knockout mice
  • Serpentine receptors
  • Traumatic brain injury

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