PMID- 12078856
OWN - NLM
STAT- MEDLINE
DCOM- 20030728
LR  - 20190922
IS  - 0271-9142 (Print)
IS  - 0271-9142 (Linking)
VI  - 22
IP  - 3
DP  - 2002 May
TI  - Induction of MCP-1 expression in airway epithelial cells: role of CCR2 receptor 
      in airway epithelial injury.
PG  - 144-52
AB  - The repair of an injured bronchial epithelial cell (BEC) monolayer requires 
      proliferation and migration of BECs into the injured area. We hypothesized that 
      BEC monolayer injury results in monocyte chemoattractant protein-1 (MCP-1) 
      production, which initiates the repair process. BECs (BEAS-2B from ATCC) were 
      utilized in this study. MCP-1 interacts with CCR2B receptor (CCR2B), resulting in 
      cell proliferation, haptotaxis, and healing of the monolayer. Reverse 
      transcriptase-polymerase chain reaction (RT-PCR) was employed to verify the 
      presence of CCR2B. CCR2B was not merely present but also inducible by 
      interleukin-2 (IL-2) and lipopolysaccharide (LPS). We demonstrated by 
      immunohistochemistry that BECs express MCP-1 after injury and that receptor 
      expression can be regulated by exposure to IL-2 and LPS. Haptotactic migration of 
      cells was enhanced in the presence of MCP-1 and reduced in the presence of CCR2B 
      antibody. This enhanced or depressed ability of the BECs to perform haptotactic 
      migration was shown to be statistically significant (P < 0.05) when compared to 
      controls. Finally, BECs proliferate in response to MCP-1 as proven by electric 
      cell-substrate impedance sensing (ECIS) technology. MCP-1-specific antibodies 
      were shown to neutralize the MCP-1-mediated BEC proliferation. This cascade of 
      events following injury to the bronchial epithelium may provide insight into the 
      mechanism of the repair process.
FAU - Lundien, Matthew C
AU  - Lundien MC
AD  - Division of Pulmonary and Critical Care Medicine, Veterans Affairs Medical 
      Center, Indiana University School of Medicine, Indianapolis 46202, USA.
FAU - Mohammed, Kamal A
AU  - Mohammed KA
FAU - Nasreen, Najmunnisa
AU  - Nasreen N
FAU - Tepper, R S
AU  - Tepper RS
FAU - Hardwick, Joyce A
AU  - Hardwick JA
FAU - Sanders, Kerry L
AU  - Sanders KL
FAU - Van Horn, Robert D
AU  - Van Horn RD
FAU - Antony, Veena B
AU  - Antony VB
LA  - eng
GR  - NIH-R01-AI45338-02/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - J Clin Immunol
JT  - Journal of clinical immunology
JID - 8102137
RN  - 0 (CCR2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-2)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Bronchi/*cytology
MH  - Cell Division
MH  - Cell Line, Transformed
MH  - Cell Movement
MH  - Chemokine CCL2/biosynthesis/*physiology
MH  - Epithelial Cells/metabolism/*pathology
MH  - Gene Expression Regulation
MH  - Humans
MH  - Interleukin-2/pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/drug effects/physiology
EDAT- 2002/06/25 10:00
MHDA- 2003/07/29 05:00
CRDT- 2002/06/25 10:00
PHST- 2002/06/25 10:00 [pubmed]
PHST- 2003/07/29 05:00 [medline]
PHST- 2002/06/25 10:00 [entrez]
AID - 10.1023/a:1015420029430 [doi]
PST - ppublish
SO  - J Clin Immunol. 2002 May;22(3):144-52. doi: 10.1023/a:1015420029430.