PMID- 9228919
OWN - NLM
STAT- MEDLINE
DCOM- 19970813
LR  - 20171116
IS  - 0022-4804 (Print)
IS  - 0022-4804 (Linking)
VI  - 70
IP  - 1
DP  - 1997 Jun
TI  - Monocyte chemoattractant protein-1 mRNA expression in the human burn wound.
PG  - 1-6
AB  - The inflammatory response following a thermal insult begins with the skin itself. 
      Langerhan's cells, tissue macrophages, keratinocytes, fibroblasts, and 
      endothelial cells contribute to the initial events of wound healing with active 
      and passive release of cell mediators. One of the mediators potentially important 
      to the repair process is monocyte chemoattractant protein-1 (MCP-1). Macrophages, 
      fibroblasts, endothelial cells, and keratinocytes can produce MCP-1 in response 
      to inflammatory stimuli. Therefore, we evaluated 10 human burn wound specimens 
      for MCP-1 mRNA using in situ hybridization. Selected specimens of different ages 
      were examined using combined in situ hybridization and immunocytochemistry to 
      identify cell types that expressed MCP-1 mRNA. Antibodies to HAM56 for 
      macrophages, CD45 for bone marrow-derived cells, Factor VIII for endothelial 
      cells, and Factor XIIIa for dermal antigen-presenting cells were included in 
      these experiments. By Postburn Day 2, basal layer keratinocytes at the edges of 
      the wound had upregulated MCP-1 message; the increased signal persisted in the 
      rate pegs deep in the dermal wound bed through 49 days postinjury. Occasional 
      FXIIIa+ immunostained dermal cells expressed MCP-1 mRNA. Islands of granulation 
      tissue throughout the wound bed were positive for increased expression of MCP-1; 
      endothelial cells and inflammatory cells both contributed to this upregulated 
      signal. Our data support the theory that the skin itself is a component of the 
      immune system and that noninflammatory cells contribute to the initiation and 
      maintenance of the inflammation at a wound site. Failure to produce MCP-1 or 
      other related mediators by indigenous cutaneous cells may delay the inflammatory 
      response to injury and potentially disrupt other essential phases of wound 
      repair.
FAU - Gibran, N S
AU  - Gibran NS
AD  - Department of Surgery, University of Washington, Seattle 98104, USA.
FAU - Ferguson, M
AU  - Ferguson M
FAU - Heimbach, D M
AU  - Heimbach DM
FAU - Isik, F F
AU  - Isik FF
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Antibodies)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, Myelomonocytic)
RN  - 0 (CD68 antigen, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (HAM-56 antibody)
RN  - 0 (RNA, Messenger)
RN  - EC 3.1.3.48 (Leukocyte Common Antigens)
SB  - IM
MH  - Antibodies
MH  - Antibodies, Monoclonal
MH  - Antigens, CD/analysis
MH  - Antigens, Differentiation, Myelomonocytic/analysis
MH  - Bone Marrow Cells
MH  - Burns/*metabolism
MH  - Chemokine CCL2/*genetics/physiology
MH  - Endothelium/metabolism
MH  - *Gene Expression
MH  - Humans
MH  - Immunohistochemistry
MH  - Immunophenotyping
MH  - In Situ Hybridization
MH  - Leukocyte Common Antigens/analysis
MH  - Macrophages/metabolism
MH  - RNA, Messenger/*metabolism
MH  - Skin/metabolism
MH  - Wound Healing
EDAT- 1997/06/01 00:00
MHDA- 1997/06/01 00:01
CRDT- 1997/06/01 00:00
PHST- 1997/06/01 00:00 [pubmed]
PHST- 1997/06/01 00:01 [medline]
PHST- 1997/06/01 00:00 [entrez]
AID - S0022-4804(97)95017-4 [pii]
AID - 10.1006/jsre.1997.5017 [doi]
PST - ppublish
SO  - J Surg Res. 1997 Jun;70(1):1-6. doi: 10.1006/jsre.1997.5017.