PMID- 9130630
OWN - NLM
STAT- MEDLINE
DCOM- 19970522
LR  - 20061115
IS  - 0014-2980 (Print)
IS  - 0014-2980 (Linking)
VI  - 27
IP  - 4
DP  - 1997 Apr
TI  - Expression and regulation of monocyte chemoattractant protein-1 by human 
      eosinophils.
PG  - 816-24
AB  - Several recent studies have identified eosinophils as a cellular source of 
      various cytokines, indicating that eosinophils play not only an effector role, 
      but also a regulatory role within the allergic inflammatory cell network. In this 
      study, we demonstrate that eosinophils can generate and secrete monocyte 
      chemoattractant protein-1 (MCP-1), a prototype of C-C chemokines. Eosinophils 
      generated immunoreactive MCP-1 in response to such diverse stimuli as C5a, 
      formyl-methionyl-leucyl-phenylalanine (FMLP) and ionomycin, but MCP-1 production 
      was not induced by interleukin (IL)-1 or tumor necrosis factor-alpha. C5a- and 
      FMLP-induced eosinophil MCP-1 production was absolutely dependent on pretreatment 
      with cytochalasin B. Eosinophils elaborated significantly more MCP-1 than 
      neutrophils. Immunoreactive MCP-1 was detected at 6 h of incubation with C5a or 
      FMLP. Expression of MCP-1 mRNA reached a maximum within the first 3 h after 
      stimulation and then declined rapidly to a very low and stable level by 18 h. 
      Pretreatment with IL-5 markedly amplified C5a-induced MCP-1 production, and the 
      enhancement occurred at the pretranslational level. Eosinophil-active chemokines 
      such as eotaxin failed to induce MCP-1 generation, even when eosinophils were 
      primed by IL-5. Since MCP-1 exerts a potent histamine-releasing effect on human 
      basophils, our results indicate that eosinophils may regulate basophil mediator 
      release with possible consequent contribution to the pathogenesis of allergic 
      inflammation via a paracrine mechanism.
FAU - Izumi, S
AU  - Izumi S
AD  - Department of Medicine and Physical Therapy, University of Tokyo School of 
      Medicine, Japan.
FAU - Hirai, K
AU  - Hirai K
FAU - Miyamasu, M
AU  - Miyamasu M
FAU - Takahashi, Y
AU  - Takahashi Y
FAU - Misaki, Y
AU  - Misaki Y
FAU - Takaishi, T
AU  - Takaishi T
FAU - Morita, Y
AU  - Morita Y
FAU - Matsushima, K
AU  - Matsushima K
FAU - Ida, N
AU  - Ida N
FAU - Nakamura, H
AU  - Nakamura H
FAU - Kasahara, T
AU  - Kasahara T
FAU - Ito, K
AU  - Ito K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Interleukin-5)
RN  - 0 (RNA, Messenger)
RN  - 80295-54-1 (Complement C5a)
SB  - IM
MH  - Chemokine CCL2/*biosynthesis/genetics/immunology
MH  - Chemokines/pharmacology
MH  - Complement C5a/agonists/pharmacology
MH  - Eosinophils/chemistry/drug effects/*immunology/*metabolism
MH  - Humans
MH  - Immunohistochemistry
MH  - Interleukin-5/agonists/pharmacology
MH  - Kinetics
MH  - Monocytes/drug effects/metabolism
MH  - Neutrophils/drug effects/metabolism
MH  - RNA, Messenger/biosynthesis
EDAT- 1997/04/01 00:00
MHDA- 1997/04/01 00:01
CRDT- 1997/04/01 00:00
PHST- 1997/04/01 00:00 [pubmed]
PHST- 1997/04/01 00:01 [medline]
PHST- 1997/04/01 00:00 [entrez]
AID - 10.1002/eji.1830270404 [doi]
PST - ppublish
SO  - Eur J Immunol. 1997 Apr;27(4):816-24. doi: 10.1002/eji.1830270404.