PMID- 10805972
OWN - NLM
STAT- MEDLINE
DCOM- 20000706
LR  - 20181130
IS  - 0008-8749 (Print)
IS  - 0008-8749 (Linking)
VI  - 201
IP  - 1
DP  - 2000 Apr 10
TI  - TGFbeta1 and TNFalpha secreted by mast cells stimulated via the FcepsilonRI 
      activate fibroblasts for high-level production of monocyte chemoattractant 
      protein-1 (MCP-1).
PG  - 42-9
AB  - Monocytes/macrophages usually make up the largest population of cells in the 
      airways of allergic asthma patients and, as such, contribute substantially to the 
      pathogenesis of this and other allergic diseases. In this report we address one 
      mechanism by which monocytes can be recruited during allergic responses. We and 
      others have shown previously that MCP-1 is important to monocyte infiltration of 
      the tissues during allergic responses in mice and, independently, that mast cells 
      activate fibroblasts to express type alpha1(I)-collagen during such responses. We 
      demonstrate herein that immunologically activated, but not quiescent mouse 
      bone-marrow-derived mast cells release mediators which in turn activate primary 
      cultures of embryonic dermal fibroblasts for high-level secretion of monocyte 
      chemoattractant activities. We identify the CC chemokine MCP-1 as a major 
      component of this activity. Anti-MCP-1 antibodies neutralized approximately 80% 
      of the monocyte chemoattractant activities secreted by such mast-cell-activated 
      fibroblasts. Furthermore, our data implicate mast cell TGFbeta and TNFalpha in 
      this process. Depletion of TGFbeta, TNFalpha, or both TGFbeta and TNFalpha from 
      the mediator pool secreted by mast cells activated via the FcepsilonRI reduced 
      the mast-cell-driven fibroblast MCP-1 response by 80+/-15, 56+/-11, or 82+/-5%, 
      respectively. These data thus further delineate a mechanism by which fibroblasts 
      are recruited into and participate in the mast cell-leukocyte cytokine cascades 
      that orchestrate allergic responses.
CI  - Copyright 2000 Academic Press.
FAU - Gordon, J R
AU  - Gordon JR
AD  - Department of Veterinary Microbiology, University of Saskatchewan, Saskatoon, S7N 
      5B4, Canada. j.r.gordon@usask.ca
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Cell Immunol
JT  - Cellular immunology
JID - 1246405
RN  - 0 (Chemokine CCL2)
RN  - 0 (Receptors, IgE)
RN  - 0 (Transforming Growth Factor alpha)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Fibroblasts/cytology/*metabolism
MH  - Gene Expression
MH  - Mast Cells/*metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Receptors, IgE/*metabolism
MH  - Skin/cytology
MH  - Transforming Growth Factor alpha/*metabolism/physiology
MH  - Transforming Growth Factor beta/*metabolism/physiology
EDAT- 2000/05/12 09:00
MHDA- 2000/07/08 11:00
CRDT- 2000/05/12 09:00
PHST- 2000/05/12 09:00 [pubmed]
PHST- 2000/07/08 11:00 [medline]
PHST- 2000/05/12 09:00 [entrez]
AID - S0008874900916319 [pii]
AID - 10.1006/cimm.2000.1631 [doi]
PST - ppublish
SO  - Cell Immunol. 2000 Apr 10;201(1):42-9. doi: 10.1006/cimm.2000.1631.