PMID- 8805671
OWN - NLM
STAT- MEDLINE
DCOM- 19961212
LR  - 20061115
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 157
IP  - 6
DP  - 1996 Sep 15
TI  - T helper 2 cytokines differently regulate monocyte chemoattractant protein-1 
      production by human peripheral blood monocytes and alveolar macrophages.
PG  - 2660-5
AB  - Th2 cytokines, such as IL-4, IL-10, and IL-13, suppress proinflammatory cytokine 
      production by monocytes/macrophages. Since monocyte chemoattractant protein-1 
      (MCP-1) is presumed to play an important role in monocyte recruitment and 
      activation during inflammatory and immune responses, we examined here the effects 
      of these Th2 cytokines on MCP-1 production by human blood monocytes and alveolar 
      macrophages. Unstimulated, highly purified blood monocytes did not produce MCP-1 
      spontaneously, while LPS treatment induced the production of MCP-1 and its mRNA 
      expression. All Th2 cytokines tested suppressed LPS-induced MCP-1 production and 
      its mRNA expression, although the suppressive effect of IL-13 was weaker than 
      that of IL-4 or IL-10. In contrast, IL-10, but neither IL-4 nor IL-13, induced 
      unstimulated peripheral blood monocytes to produce biologically active MCP-1 
      protein within 4 h, reaching a maximal level at 12 h. IL-10-induced MCP-1 
      production was reduced by pretreatment of IL-10 with anti-IL-10 Ab, negating the 
      involvement of contaminated endotoxin. Moreover, IL-10 induced MCP-1 mRNA 
      expression in unstimulated monocytes, independent of de novo protein synthesis. 
      Furthermore, human alveolar macrophages produced MCP-1 spontaneously, and the 
      production was inhibited by IL-4 or IL-13, but was augmented by IL-10. These 
      findings suggest that IL-10 regulates MCP-1 production by monocytes/macrophages 
      in a different way from other Th2 cytokines, such as IL-4 and IL-13, and 
      contributes to host defense responses.
FAU - Yano, S
AU  - Yano S
AD  - Third Department of Internal Medicine, University of Tokushima School of 
      Medicine, Japan.
FAU - Yanagawa, H
AU  - Yanagawa H
FAU - Nishioka, Y
AU  - Nishioka Y
FAU - Mukaida, N
AU  - Mukaida N
FAU - Matsushima, K
AU  - Matsushima K
FAU - Sone, S
AU  - Sone S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis
MH  - Cytokines/*analysis/*pharmacology
MH  - Humans
MH  - Leukocytes/metabolism
MH  - Macrophages, Alveolar/*drug effects/*metabolism
MH  - Monocytes/*drug effects/*metabolism
MH  - Th2 Cells/*immunology
EDAT- 1996/09/15 00:00
MHDA- 1996/09/15 00:01
CRDT- 1996/09/15 00:00
PHST- 1996/09/15 00:00 [pubmed]
PHST- 1996/09/15 00:01 [medline]
PHST- 1996/09/15 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1996 Sep 15;157(6):2660-5.