PMID- 7891256
OWN - NLM
STAT- MEDLINE
DCOM- 19950420
LR  - 20220330
IS  - 0022-3492 (Print)
IS  - 0022-3492 (Linking)
VI  - 66
IP  - 1
DP  - 1995 Jan
TI  - Fibroblasts, mononuclear phagocytes, and endothelial cells express monocyte 
      chemoattractant protein-1 (MCP-1) in inflamed human gingiva.
PG  - 80-8
AB  - Gingival inflammation is initiated by bacterial colonization of the tooth 
      surface. It is characterized by infiltration of mononuclear cells, a feature of 
      many forms of chronic inflammation. Monocyte chemoattractant protein-1 (MCP-1) is 
      the predominant monocyte chemoattractant secreted by a variety of cells in vitro. 
      We examined MCP-1 expression in chronic gingival inflammation by double antibody 
      immunohistochemistry that utilized rabbit anti-MCP-1 antibody simultaneously with 
      mouse monoclonal antibodies to specific cellular markers. MCP-1 mRNA expression 
      by fibroblasts in inflamed gingival tissues was examined by in situ 
      hybridization. We report here that in human chronic gingival inflammation the 
      principal cell type expressing MCP-1 in dense inflammatory infiltrates is the 
      mononuclear phagocyte. The cells expressing MCP-1 in moderately inflamed areas 
      and in adjacent areas to inflammatory infiltrates are mononuclear phagocytes and 
      fibroblasts, while in areas of fibroblastic hyperplasia, MCP-1 positive cells are 
      predominantly fibroblasts. We also demonstrate that in moderately and highly 
      inflamed areas, the extent of MCP-1 expression is greater than that in adjacent 
      normal/mildly inflamed areas. As the degree of inflammation increased, there is 
      also a concomitant increase in the number of mononuclear phagocytes. Furthermore, 
      it is apparent that most of the infiltrating monocytes/macrophages are positive 
      for MCP-1 in vivo. Our finding that MCP-1 expression is unambiguously identified 
      in fibroblasts suggests that they can play a role in host defense by initiating 
      the recruitment of monocytes. In addition, the expression of chemokines such as 
      MCP-1 may represent a mechanism for amplification of inflammatory signals in 
      gingival inflammation.
FAU - Yu, X
AU  - Yu X
AD  - Department of Periodontology and Oral Biology, Boston University School of 
      Graduate Dentistry, MA, USA.
FAU - Graves, D T
AU  - Graves DT
LA  - eng
GR  - DE07559/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Periodontol
JT  - Journal of periodontology
JID - 8000345
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (DNA, Antisense)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*biosynthesis/immunology
MH  - Chemotaxis, Leukocyte
MH  - Chronic Disease
MH  - Cytokines/biosynthesis
MH  - DNA, Antisense
MH  - Endothelium, Vascular/cytology/metabolism
MH  - Fibroblasts/immunology/metabolism
MH  - Gingivitis/*immunology/pathology
MH  - Humans
MH  - Immunohistochemistry/methods
MH  - In Situ Hybridization
MH  - Macrophages/immunology/metabolism
MH  - Mice
MH  - Monocytes/immunology/metabolism
MH  - RNA, Messenger/analysis
MH  - Rabbits
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
AID - 10.1902/jop.1995.66.1.80 [doi]
PST - ppublish
SO  - J Periodontol. 1995 Jan;66(1):80-8. doi: 10.1902/jop.1995.66.1.80.