PMID- 1386129
OWN - NLM
STAT- MEDLINE
DCOM- 19920826
LR  - 20190725
IS  - 0085-2538 (Print)
IS  - 0085-2538 (Linking)
VI  - 42
IP  - 1
DP  - 1992 Jul
TI  - IL-1 receptor antagonist inhibits monocyte chemotactic peptide 1 generation by 
      human mesangial cells.
PG  - 95-101
AB  - The elicitation of neutrophils and monocytes from the circulation into the 
      inflamed glomerulus is a key process in the pathogenesis of proliferative 
      glomerulonephritis. The aim of this study was to determine the factors which 
      regulate the expression and synthesis of the monocyte specific chemotaxin, 
      monocyte chemotactic peptide 1 (MCP-1). Mesangial cells in culture did not 
      constitutively express MCP-1, but could be induced to express both MCP-1 mRNA and 
      antigenic MCP-1 by either stimulation with IL-1 alpha or TNF alpha, which are 
      also stimuli for interleukin 8 (IL-8/NAP-1) expression and release. Pre-treatment 
      of mesangial cells with the IL-1 receptor antagonist (IL-1ra) induced 
      dose-dependent inhibition of both the expression of MCP-1 and IL-8 mRNA as well 
      as the release of both chemotactic peptides in response to IL-1 alpha, while the 
      receptor antagonist had no significant effect on TNF alpha induced MCP-1 and IL-8 
      generation. This study demonstrates that the IL-1 receptor antagonist was four 
      times more effective at inhibiting the IL-1 induced expression and release of 
      IL-8 compared to that of MCP-1. These results suggest that mesangial cell-derived 
      MCP-1 may play an important role in the recruitment of monocytes in glomerular 
      inflammation and that an IL-1 receptor antagonist may have therapeutic potential 
      for the treatment of glomerulonephritis.
FAU - Brown, Z
AU  - Brown Z
AD  - Department of Pharmacology, University of Bath, Avon, England, United Kingdom.
FAU - Strieter, R M
AU  - Strieter RM
FAU - Neild, G H
AU  - Neild GH
FAU - Thompson, R C
AU  - Thompson RC
FAU - Kunkel, S L
AU  - Kunkel SL
FAU - Westwick, J
AU  - Westwick J
LA  - eng
GR  - DK-38149/DK/NIDDK NIH HHS/United States
GR  - HL-2576/HL/NHLBI NIH HHS/United States
GR  - Wellcome Trust/United Kingdom
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  - Kidney Int
JT  - Kidney international
JID - 0323470
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (DNA Probes)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Immunologic)
RN  - 0 (Receptors, Interleukin-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Base Sequence
MH  - Cells, Cultured
MH  - Chemokine CCL2
MH  - Chemotactic Factors/*biosynthesis/genetics
MH  - DNA/genetics
MH  - DNA Probes
MH  - Gene Expression
MH  - Glomerular Mesangium/immunology/*metabolism
MH  - Humans
MH  - Interleukin-1/pharmacology
MH  - Interleukin-8/biosynthesis/genetics
MH  - Molecular Sequence Data
MH  - RNA, Messenger/genetics/metabolism
MH  - Receptors, Immunologic/*antagonists & inhibitors
MH  - Receptors, Interleukin-1
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 1992/07/01 00:00
MHDA- 1992/07/01 00:01
CRDT- 1992/07/01 00:00
PHST- 1992/07/01 00:00 [pubmed]
PHST- 1992/07/01 00:01 [medline]
PHST- 1992/07/01 00:00 [entrez]
AID - S0085-2538(15)57695-3 [pii]
AID - 10.1038/ki.1992.266 [doi]
PST - ppublish
SO  - Kidney Int. 1992 Jul;42(1):95-101. doi: 10.1038/ki.1992.266.