PMID- 12771503 OWN - NLM STAT- MEDLINE DCOM- 20031117 LR - 20171101 IS - 0250-8095 (Print) IS - 0250-8095 (Linking) VI - 23 IP - 4 DP - 2003 Jul-Aug TI - Direct contact between human peripheral blood mononuclear cells and renal fibroblasts facilitates the expression of monocyte chemoattractant protein-1. PG - 208-13 AB - BACKGROUND: Cell-to-cell interaction is thought to be an important feature of a variety of biological processes. As far as the proinflammatory process is concerned, the interaction between mesangial cells and monocytes/macrophages induces the expression of monocyte chemoattractant protein-1 (MCP-1), and this may play a role in glomerulonephritis. In this study, we investigated whether the cell-to-cell interaction between immune cells and renal fibroblasts induces MCP-1 gene expression, which may be involved in interstitial inflammation in the kidney. METHODS: Human renal fibroblast cell lines, tNKF (from a normal kidney) and tFKIF (from a kidney with fibrosis), and peripheral blood mononuclear cells (PBMC) were used to assess the effect of cell-to-cell contact on the expression of MCP-1 mRNA in the fibroblasts. The expression of the MCP-1 gene in the fibroblasts was also examined after stimulation with tumor necrosis factor-alpha (TNF-alpha) and the culture supernatant from PBMC. RT-PCR was used to detect MCP-1 mRNA expression. Neutralizing antibodies to intercellular adhesion molecule-1 (ICAM-1) and vascular endothelial adhesion molecule-1 (VCAM-1) were used to block the cell-to-cell contact between the fibroblasts and PBMC. RESULTS: TNF-alpha and the culture supernatant from PBMC increased MCP-1 gene expression in tNKF cells. Contact culture with PBMC also significantly increased MCP-1 gene expression in tNKF cells. Although the basal level of MCP-1 mRNA was higher in tFKIF than tNKF cells, tFKIF cells did not respond significantly to any stimulation in this study. Following pretreatment with anti-ICAM-1 antibody, MCP-1 gene expression in tNKF cells was significantly suppressed in contact culture with PBMC. Anti-VCAM-1 antibody treatment had no effects. CONCLUSION: It is suggested that the interaction between renal fibroblasts and PBMC was mediated through direct contact and by secreted humoral factors. ICAM-1 on renal fibroblasts may be involved in the direct cell-to-cell interaction inducing MCP-1 gene expression, which seems to be involved in renal interstitial inflammation. CI - Copyright 2003 S. Karger AG, Basel FAU - Hao, Lirong AU - Hao L AD - Department of Nephrology, Saitama Medical School, Irumagun, Saitama, Japan. FAU - Okada, Hirokazu AU - Okada H FAU - Kanno, Yoshihiko AU - Kanno Y FAU - Inoue, Tsutomu AU - Inoue T FAU - Kobayashi, Tatsuya AU - Kobayashi T FAU - Watanabe, Yusuke AU - Watanabe Y FAU - Strutz, Frank AU - Strutz F FAU - Muller, Gerhard A AU - Muller GA FAU - Suzuki, Hiromichi AU - Suzuki H LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20030527 PL - Switzerland TA - Am J Nephrol JT - American journal of nephrology JID - 8109361 RN - 0 (Antibodies) RN - 0 (Chemokine CCL2) RN - 0 (RNA, Messenger) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (Vascular Cell Adhesion Molecule-1) RN - 126547-89-5 (Intercellular Adhesion Molecule-1) SB - IM MH - Antibodies/pharmacology MH - *Cell Communication MH - Cell Line MH - Chemokine CCL2/genetics/*metabolism MH - Coculture Techniques MH - Fibroblasts/cytology/*metabolism MH - Humans MH - Intercellular Adhesion Molecule-1/immunology MH - Kidney/*cytology MH - Leukocytes, Mononuclear/*cytology MH - RNA, Messenger/metabolism MH - Tumor Necrosis Factor-alpha/pharmacology MH - Vascular Cell Adhesion Molecule-1/immunology EDAT- 2003/05/29 05:00 MHDA- 2003/12/03 05:00 CRDT- 2003/05/29 05:00 PHST- 2003/03/20 00:00 [received] PHST- 2003/04/23 00:00 [accepted] PHST- 2003/05/29 05:00 [pubmed] PHST- 2003/12/03 05:00 [medline] PHST- 2003/05/29 05:00 [entrez] AID - 71480 [pii] AID - 10.1159/000071480 [doi] PST - ppublish SO - Am J Nephrol. 2003 Jul-Aug;23(4):208-13. doi: 10.1159/000071480. Epub 2003 May 27.