PMID- 9792337
OWN - NLM
STAT- MEDLINE
DCOM- 19981223
LR  - 20181113
IS  - 0962-9351 (Print)
IS  - 0962-9351 (Linking)
VI  - 7
IP  - 4
DP  - 1998
TI  - Differential regulation of C-C chemokines during fibroblast-monocyte 
      interactions: adhesion vs. inflammatory cytokine pathways.
PG  - 269-74
AB  - The cell-to-cell interactions during chronic inflammatory diseases likely 
      contribute to leukocyte accumulation leading to increased pathology and organ 
      dysfunction. In particular, there is a paucity of information relating to the 
      maintenance of chronic fibrotic diseases. Using a lung fibroblast line and 
      enriched monocyte populations, we have investigated the activational events which 
      contribute to the production of two C-C chemokines, macrophage inflammatory 
      protein-1 alpha (MIP-1alpha) and monocyte chemoattractant protein-1 (MCP-1), 
      during fibroblast-monocyte interactions. Neither the fibroblast cell line (16lu) 
      nor isolated monocytes alone produced significant levels of MIP-1alpha or MCP-1. 
      However, when isolated monocytes were layered onto 16 lu fibroblast monolayers a 
      significant increase in MIP-1alpha and MCP-1 production was observed. The use of 
      fixed cell populations indicated that the MIP-1alpha was derived from monocytes 
      and MCP-1 from both cell populations. To examine the molecules which were 
      required for chemokine production during the interaction, specific antibodies 
      were used in the co-cultures. Blocking beta3-integrin interactions significantly 
      inhibited MIP-1alpha production. In contrast, beta-integrin interactions had no 
      effect on the MCP-1 production, while, neutralization of TNF significantly 
      decreased MCP-1 production during the co-culture. These data indicate that 
      fibroblast-monocyte interactions induce chemokine production through different 
      mechanisms and a combination of these responses may contribute to the maintenance 
      of the mononuclear cell accumulation during disease progression.
FAU - Zickus, C
AU  - Zickus C
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor 
      48109-0602, USA.
FAU - Kunkel, S L
AU  - Kunkel SL
FAU - Simpson, K
AU  - Simpson K
FAU - Evanoff, H
AU  - Evanoff H
FAU - Glass, M
AU  - Glass M
FAU - Strieter, R M
AU  - Strieter RM
FAU - Lukacs, N W
AU  - Lukacs NW
LA  - eng
GR  - AI36302/AI/NIAID NIH HHS/United States
GR  - HL59178/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mediators Inflamm
JT  - Mediators of inflammation
JID - 9209001
RN  - 0 (Chemokines, CC)
RN  - 0 (Cytokines)
RN  - 0 (Integrin beta1)
SB  - IM
MH  - Cell Adhesion
MH  - *Cell Communication
MH  - Cells, Cultured
MH  - Chemokines, CC/*biosynthesis
MH  - Cytokines/*physiology
MH  - Fibroblasts/*physiology
MH  - Humans
MH  - Inflammation/immunology
MH  - Integrin beta1/physiology
MH  - Monocytes/*physiology
PMC - PMC1781852
EDAT- 1998/10/29 00:00
MHDA- 1998/10/29 00:01
PMCR- 1998/01/01
CRDT- 1998/10/29 00:00
PHST- 1998/10/29 00:00 [pubmed]
PHST- 1998/10/29 00:01 [medline]
PHST- 1998/10/29 00:00 [entrez]
PHST- 1998/01/01 00:00 [pmc-release]
AID - 10.1080/09629359890956 [doi]
PST - ppublish
SO  - Mediators Inflamm. 1998;7(4):269-74. doi: 10.1080/09629359890956.