PMID- 11985519
OWN - NLM
STAT- MEDLINE
DCOM- 20020614
LR  - 20190513
IS  - 0009-9104 (Print)
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Linking)
VI  - 128
IP  - 2
DP  - 2002 May
TI  - IFNgamma induces functional chemokine receptor expression in human mesangial 
      cells.
PG  - 285-94
AB  - Infiltration of leucocyte populations into sites of inflammation is a common 
      feature in renal diseases. Glomerular mesangial cells are potent producers of a 
      variety of chemokines, leading to specific attraction of distinct types of 
      inflammatory leucocytes into the glomerulus, but so far there is limited 
      knowledge about the responsiveness of mesangial cells to chemokines. We 
      investigated the expression of chemokine receptors and the responsiveness of 
      primary human mesangial cells (HMC) to the chemokines which they produce, namely 
      monocyte chemoattractant protein-1 (MCP-1) and interleukin (IL)-8. We found that 
      mRNAs of the chemokine receptors CCR1, which has been shown before, CCR2 and 
      CXCR2 were induced by T-helper cytokine interferon-gamma (IFNgamma). In 
      IFNgamma-stimulated cells, CCR2 and CXCR2 were detectable by flow cytometry. 
      Following treatment with IFNgamma, HMC responded to MCP-1 and IL-8 with an 
      increase of IL-6 mRNA and protein expression, which was in part blocked by 
      pertussis toxin. Moreover, chemokine stimulation of transfected HMC led to an 
      activation of the immunoregulatory transcription factors NFkappaB and AP-1. 
      Additionally, we found that MCP-1 enhanced the expression of its own mRNA in 
      cells activated to express CCR2, suggesting autocrine feedback mechanisms in 
      MCP-1 regulation. Finally, IFNgamma-activated cells migrated towards an MCP-1 
      gradient in a chemotaxis assay. These results strengthen the assumption that 
      chemokines are not only involved in the recruitment of immune cells to inflamed 
      tissues, but also seem to play a central role in the autocrine regulation of 
      local tissue cells, leading to proceeding inflammation and possibly contributing 
      to healing by mediating cell growth and migration.
FAU - Schwarz, M
AU  - Schwarz M
AD  - pharmazentrum frankfurt, Hospital of the Johann Wolfgang Goethe University, 
      Frankfurt am Main, Germany.
FAU - Wahl, M
AU  - Wahl M
FAU - Resch, K
AU  - Resch K
FAU - Radeke, H H
AU  - Radeke HH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (CCR1 protein, human)
RN  - 0 (CCR2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR1)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (Receptors, Interleukin-8B)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Autocrine Communication/immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism/pharmacology
MH  - Chemotaxis/drug effects
MH  - Glomerular Mesangium/immunology/*metabolism
MH  - Humans
MH  - Interferon-gamma/immunology/*pharmacology
MH  - Interleukin-8/metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Receptors, CCR1
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/*biosynthesis
MH  - Receptors, Interleukin-8B/*biosynthesis
MH  - T-Lymphocytes, Helper-Inducer/immunology
MH  - Up-Regulation/drug effects/immunology
PMC - PMC1906381
EDAT- 2002/05/03 10:00
MHDA- 2002/06/18 10:01
PMCR- 2003/05/01
CRDT- 2002/05/03 10:00
PHST- 2002/05/03 10:00 [pubmed]
PHST- 2002/06/18 10:01 [medline]
PHST- 2002/05/03 10:00 [entrez]
PHST- 2003/05/01 00:00 [pmc-release]
AID - 1829 [pii]
AID - 10.1046/j.1365-2249.2002.01829.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2002 May;128(2):285-94. doi: 10.1046/j.1365-2249.2002.01829.x.