Selective chemokine mRNA accumulation in the rat spinal cord after contusion injury

✍ Scribed by Dana M. McTigue; Marie Tani; Kimberly Krivacic; Ann Chernosky; Gregory S. Kelner; Dominique Maciejewski; Richard Maki; Richard M. Ransohoff; Bradford T. Stokes

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 132 KB
• Volume: 53
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/(sici)1097-4547(19980801)53:3<368::aid-jnr11>3.0.co;2-1

✦ Synopsis

Following traumatic injury to the spinal cord, hematogenous inflammatory cells including neutrophils, monocytes, and lymphocytes infiltrate the lesion in a distinct temporal sequence. To examine potential mechanisms for their recruitment, we measured chemokine mRNAs in the contused rat spinal cord, using specific and sensitive reverse transcriptase polymerase chain reaction (RT-PCR) dot-blot hybridization assays. The neutrophil chemoattractant GRO-␣ was 30-fold higher than control values at 6 hr postinjury and decayed rapidly thereafter. LIX, a highly related ␣-chemokine, also was elevated early postinjury. Monocyte chemoattractant peptide (MCP)-1 and MCP-5 mRNAs, potent chemoattractants for monocytes, were significantly elevated at the lesion epicenter at 12 and 24 hr postinjury and declined thereafter. Interferon-␥-inducible protein, 10 kDa (IP-10), chemoattractant towards activated Tlymphocytes, was significantly elevated at 6 and 12 hr postinjury. The dendritic cell chemoattractant MIP-3␣ also was increased, perhaps contributing to the development of T-cell autoreactivity to neural components after spinal cord injury (SCI) in rats. Other ␤-chemokines, including MIP-1␣ and RANTES (regulated on expression normal T-cell expressed and secreted), were minimally affected by SCI. Expression of chemokines, therefore, directly precedes the influx of target neutrophils, monocytes, and T-cells into the spinal cord postinjury, as noted previously. Thus, selective chemokine expression may be integral to inflammatory processes within the injured spinal cord as a mechanism of recruitment for circulating leukocytes.