PMID- 11350637
OWN - NLM
STAT- MEDLINE
DCOM- 20010726
LR  - 20220321
IS  - 1067-1927 (Print)
IS  - 1067-1927 (Linking)
VI  - 9
IP  - 1
DP  - 2001 Jan-Feb
TI  - Modulation of macrophage recruitment into wounds by monocyte chemoattractant 
      protein-1.
PG  - 28-33
AB  - Previous studies suggest that normal wound repair requires the regulated 
      production of monocyte and macrophage chemoattractants. The current study 
      examines the role of monocyte chemoattractant protein-1 (MCP-1) in coordinating 
      monocyte recruitment into sites of injury. MCP-1 protein was detected in both 
      incisional and excisional murine wounds, with a peak concentration occurring 
      slightly before maximum macrophage infiltration. Compared to wounds treated with 
      control antibody, wounds treated with a neutralizing monoclonal anti-MCP-1 
      antibody contained significantly fewer macrophages (8.2 +/- 0.9 vs. 14 +/- 1.7 
      macrophages per high power field, p < 0.05). Conversely, the addition of 
      recombinant MCP-1 to wounds resulted in a substantial increase in the number of 
      macrophages (107% to 124% increase over untreated wounds, p < 0.01). Because 
      macrophages promote wound healing, the effect of recombinant MCP-1 on the wound 
      healing process was examined. Incisional wounds (n = 12) were either left 
      untreated or treated with vehicle alone, 5 ng recombinant MCP-1 in vehicle, or 50 
      ng recombinant MCP-1 in vehicle. Wound disruption strength was determined on days 
      7, 14, 21, and 28 for each group. Wounds treated with MCP-1 exhibited a slight 
      increase in wound disruption strength at nearly all time points but this increase 
      did not reach statistical significance. Addition of 100 ng of MCP-1 to excisional 
      wounds did not have any significant effect on wound reepithelialization. Taken 
      together, the results show that MCP-1 is produced within wounds at physiologic 
      concentrations, and is an important positive regulator of macrophage recruitment 
      into sites of injury. Addition of exogenous MCP-1 to wounds of normal mice yields 
      only modest enhancement of the repair process.
FAU - Dipietro, L A
AU  - Dipietro LA
AD  - Burn and Shock Trauma Institute, Department of Surgery, Loyola University Medical 
      Center, Maywood, Illinois 60153, USA. ldipiet@luc.edu
FAU - Reintjes, M G
AU  - Reintjes MG
FAU - Low, Q E
AU  - Low QE
FAU - Levi, B
AU  - Levi B
FAU - Gamelli, R L
AU  - Gamelli RL
LA  - eng
GR  - GM42577/GM/NIGMS NIH HHS/United States
GR  - GM55238/GM/NIGMS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Wound Repair Regen
JT  - Wound repair and regeneration : official publication of the Wound Healing Society 
      [and] the European Tissue Repair Society
JID - 9310939
RN  - 0 (Chemokine CCL2)
RN  - 0 (Recombinant Proteins)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/*metabolism/pharmacology
MH  - Disease Models, Animal
MH  - Female
MH  - Macrophages/drug effects/*metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Neutrophil Infiltration/drug effects/physiology
MH  - Recombinant Proteins/pharmacology
MH  - Reference Values
MH  - Sensitivity and Specificity
MH  - Skin/*injuries
MH  - *Wound Healing/drug effects
MH  - Wounds, Penetrating/drug therapy/*metabolism
EDAT- 2001/05/15 10:00
MHDA- 2001/07/28 10:01
CRDT- 2001/05/15 10:00
PHST- 2001/05/15 10:00 [pubmed]
PHST- 2001/07/28 10:01 [medline]
PHST- 2001/05/15 10:00 [entrez]
AID - wrr028 [pii]
AID - 10.1046/j.1524-475x.2001.00028.x [doi]
PST - ppublish
SO  - Wound Repair Regen. 2001 Jan-Feb;9(1):28-33. doi: 
      10.1046/j.1524-475x.2001.00028.x.