Selective chemokine mRNA accumulation in the rat spinal cord after contusion injury.
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-alpha was 30-fold higher than control values at 6 hr postinjury and decayed rapidly thereafter. LIX, a highly related alpha-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-gamma-inducible protein, 10 kDa (IP-10), chemoattractant towards activated T-lymphocytes, was significantly elevated at 6 and 12 hr postinjury. The dendritic cell chemoattractant MIP-3alpha also was increased, perhaps contributing to the development of T-cell autoreactivity to neural components after spinal cord injury (SCI) in rats. Other beta-chemokines, including MIP-1alpha 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.
McTigue
D M
DM
Department of Physiology, College of Medicine and Public Health, Ohio State University, Columbus 43210, USA.
Tani
M
M
Krivacic
K
K
Chernosky
A
A
Kelner
G S
GS
Maciejewski
D
D
Maki
R
R
Ransohoff
R M
RM
Stokes
B T
BT
D000818:Animals; D017951:Antigen Presentation / Q000276:immunology; D018932:Chemokine CCL2 / Q000235:genetics; D054418:Chemokine CCL20; D018946:Chemokine CCL5 / Q000235:genetics; D054360:Chemokine CXCL1; D054365:Chemokine CXCL5; D019742:Chemokines, CC; D019743:Chemokines, CXC / Q000235:genetics*; D002630:Chemotactic Factors / Q000235:genetics; D003288:Contusions / Q000378:metabolism*; D005260:Female; D015870:Gene Expression / Q000276:immunology; D006131:Growth Inhibitors / Q000235:genetics; D006133:Growth Substances / Q000235:genetics; D036341:Intercellular Signaling Peptides and Proteins; D019402:Macrophage Inflammatory Proteins / Q000235:genetics; D018945:Monocyte Chemoattractant Proteins / Q000235:genetics; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D054399:Receptors, CCR6; D019707:Receptors, Chemokine; D013119:Spinal Cord Injuries / Q000276:immunology* / Q000378:metabolism*; D013601:T-Lymphocytes / Q000276:immunology; D013997:Time Factors
C108355:CCL20 protein, human; C106311:CCR6 protein, human; C475829:CXCL1 protein, human; C486263:CXCL5 protein, human; C491224:Ccl12 protein, mouse; C103558:Ccl12 protein, rat; D018932:Chemokine CCL2; D054418:Chemokine CCL20; D018946:Chemokine CCL5; D054360:Chemokine CXCL1; D054365:Chemokine CXCL5; D019742:Chemokines, CC; D019743:Chemokines, CXC; D002630:Chemotactic Factors; C513297:Cxcl1 protein, rat; D006131:Growth Inhibitors; D006133:Growth Substances; D036341:Intercellular Signaling Peptides and Proteins; D019402:Macrophage Inflammatory Proteins; D018945:Monocyte Chemoattractant Proteins; D012333:RNA, Messenger; D054399:Receptors, CCR6; D019707:Receptors, Chemokine