PMID- 7806062
OWN - NLM
STAT- MEDLINE
DCOM- 19950201
LR  - 20220408
IS  - 0016-5085 (Print)
IS  - 0016-5085 (Linking)
VI  - 108
IP  - 1
DP  - 1995 Jan
TI  - Monocyte-chemoattractant protein 1 gene expression in intestinal epithelial cells 
      and inflammatory bowel disease mucosa.
PG  - 40-50
AB  - BACKGROUND: Monocyte-chemoattractant protein 1 (MCP-1) activates macrophages and 
      increases the migration of monocytes into tissue during inflammation. It was 
      hypothesized that MCP-1 expression is involved in intestinal inflammation. 
      METHODS: MCP-1 protein was detected by immunohistochemistry and 
      immunoprecipitation. Biological activity of MCP-1 was assessed using a 
      chemotactic assay. MCP-1 messenger RNA (mRNA) levels were measured by 
      quantitative reverse-transcription polymerase chain reaction. RESULTS: In normal 
      mucosa, MCP-1 was predominantly present in surface epithelium. In contrast, 
      inflamed mucosa from patients with ulcerative colitis or Crohn's disease 
      contained multiple cells immunoreactive for MCP-1, including spindle cells, 
      mononuclear cells, and endothelial cells. Furthermore, MCP-1 mRNA expression was 
      markedly increased in inflamed intestinal biopsy specimens from patients with 
      inflammatory bowel disease. MCP-1 was detected in isolated intestinal epithelial 
      cells and in conditioned media from Caco-2 cells. Caco-2 cell-conditioned media 
      stimulated monocyte chemotaxis activity that was inhibited by anti-MCP-1 
      antibodies. Constituitive MCP-1 mRNA levels in Caco-2 cells were up-regulated by 
      interleukin 1 beta and down-regulated by dexamethasone. CONCLUSIONS: In addition 
      to lamina propria macrophages, endothelial cells, and spindle cells, intestinal 
      epithelial cells are able to produce MCP-1. MCP-1 is expressed constitutively in 
      the intestinal colonic mucosa and is up-regulated during inflammation.
FAU - Reinecker, H C
AU  - Reinecker HC
AD  - Division of Gastroenterology, University of Pennsylvania Medical Center, 
      Philadelphia.
FAU - Loh, E Y
AU  - Loh EY
FAU - Ringler, D J
AU  - Ringler DJ
FAU - Mehta, A
AU  - Mehta A
FAU - Rombeau, J L
AU  - Rombeau JL
FAU - MacDermott, R P
AU  - MacDermott RP
LA  - eng
GR  - DK-21474/DK/NIDDK NIH HHS/United States
GR  - DK-43351/DK/NIDDK NIH HHS/United States
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  - Gastroenterology
JT  - Gastroenterology
JID - 0374630
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Molecular Probes)
RN  - 0 (RNA, Messenger)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Base Sequence
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*genetics/metabolism
MH  - Colon/metabolism
MH  - Cytokines/genetics/metabolism
MH  - Enteritis/metabolism
MH  - *Gene Expression
MH  - Humans
MH  - Inflammatory Bowel Diseases/*genetics/pathology
MH  - Interleukin-1/pharmacology
MH  - Intestinal Mucosa/pathology/*physiopathology
MH  - Molecular Probes/genetics
MH  - Molecular Sequence Data
MH  - Neoplasms, Glandular and Epithelial/metabolism/pathology
MH  - RNA, Messenger/metabolism
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Tumor Cells, Cultured
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 - 0016-5085(95)90006-3 [pii]
AID - 10.1016/0016-5085(95)90006-3 [doi]
PST - ppublish
SO  - Gastroenterology. 1995 Jan;108(1):40-50. doi: 10.1016/0016-5085(95)90006-3.