PMID- 1281207
OWN - NLM
STAT- MEDLINE
DCOM- 19930108
LR  - 20210102
IS  - 0022-1007 (Print)
IS  - 1540-9538 (Electronic)
IS  - 0022-1007 (Linking)
VI  - 176
IP  - 6
DP  - 1992 Dec 1
TI  - RANTES and macrophage inflammatory protein 1 alpha induce the migration and 
      activation of normal human eosinophil granulocytes.
PG  - 1489-95
AB  - The cellular infiltrates of certain inflammatory processes found in parasitic 
      infection or in allergic diseases consist predominantly of eosinophilic 
      granulocytes, often in association with activated T cells. This suggests the 
      existence of chemotactic agonists specific for eosinophils and lymphocyte subsets 
      devoid of neutrophil-activating properties. We therefore examined four members of 
      the intercrine/chemokine superfamily of cytokines (monocyte chemotactic peptide 1 
      [MCP-1], RANTES, macrophage inflammatory protein 1 alpha [MIP-1 alpha], and MIP-1 
      beta), which do not activate neutrophils, for their ability to affect different 
      eosinophil effector functions. RANTES strongly attracted normal human eosinophils 
      by a chemotactic rather than a chemokinetic mechanism with a similar efficacy as 
      the most potent chemotactic myeloid cell agonist, C5a. MIP-1 alpha also induced 
      eosinophil migration, however, with lower efficacy. RANTES and MIP-1 alpha 
      induced eosinophil cationic protein release in cytochalasin B-treated 
      eosinophils, but did not promote leukotriene C4 formation by eosinophils, even 
      after preincubation with interleukin 3 (IL-3), in contrast to other chemotactic 
      agonists such as C5a and formyl-methionyl-leucyl-phenylalanine (FMLP). RANTES, 
      but not MIP-1 alpha, induced a biphasic chemiluminescence response, however, of 
      lower magnitude than C5a. RANTES and MIP-1 alpha both promoted identical 
      transient changes in intracellular free calcium concentration ([Ca2+]i), with 
      kinetics similar to those induced by chemotactic peptides known to interact with 
      G protein-coupled receptors. No cross-desensitization towards other peptide 
      agonists (e.g., C5a, IL-8, FMLP) was observed, suggesting the presence of 
      specific receptors. Despite its weaker eosinophil-activating properties, MIP-1 
      alpha was at least 10 times more potent on a molar basis than RANTES at inducing 
      [Ca2+]i changes. Interestingly, RANTES deactivated the MIP-1 alpha-induced 
      [Ca2+]i changes, while the RANTES response was preserved after MIP-1 alpha 
      stimulation. MCP-1, a potent monocyte chemoattractant and basophil agonist, as 
      well as MIP-1 beta, a peptide with pronounced homology to MIP-1 alpha, did not 
      activate the eosinophil functions tested. Our results indicate that RANTES and 
      MIP-1 alpha are crucial mediators of inflammatory processes in which eosinophils 
      predominate.
FAU - Rot, A
AU  - Rot A
AD  - Institute of Clinical Immunology, Bern, Switzerland.
FAU - Krieger, M
AU  - Krieger M
FAU - Brunner, T
AU  - Brunner T
FAU - Bischoff, S C
AU  - Bischoff SC
FAU - Schall, T J
AU  - Schall TJ
FAU - Dahinden, C A
AU  - Dahinden CA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Exp Med
JT  - The Journal of experimental medicine
JID - 2985109R
RN  - 0 (Blood Proteins)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Cytokines)
RN  - 0 (Eosinophil Granule Proteins)
RN  - 0 (Lymphokines)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Monokines)
RN  - 0 (Recombinant Proteins)
RN  - 0 (SRS-A)
RN  - 11062-77-4 (Superoxides)
RN  - 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine)
RN  - 80295-54-1 (Complement C5a)
RN  - EC 3.1.- (Ribonucleases)
SB  - IM
MH  - Blood Proteins/biosynthesis
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemokine CCL5
MH  - Chemotaxis, Leukocyte/*drug effects
MH  - Complement C5a/pharmacology
MH  - Cytokines/*pharmacology
MH  - Eosinophil Granule Proteins
MH  - Eosinophils/drug effects/*physiology
MH  - Escherichia coli/genetics
MH  - Humans
MH  - In Vitro Techniques
MH  - Kinetics
MH  - Luminescent Measurements
MH  - Lymphokines/*pharmacology
MH  - Macrophage Inflammatory Proteins
MH  - Monokines/*pharmacology
MH  - N-Formylmethionine Leucyl-Phenylalanine/pharmacology
MH  - Recombinant Proteins/pharmacology
MH  - *Ribonucleases
MH  - SRS-A/biosynthesis/blood
MH  - Superoxides/blood
PMC - PMC2119467
EDAT- 1992/12/01 00:00
MHDA- 1992/12/01 00:01
PMCR- 1993/06/01
CRDT- 1992/12/01 00:00
PHST- 1992/12/01 00:00 [pubmed]
PHST- 1992/12/01 00:01 [medline]
PHST- 1992/12/01 00:00 [entrez]
PHST- 1993/06/01 00:00 [pmc-release]
AID - 93094751 [pii]
AID - 10.1084/jem.176.6.1489 [doi]
PST - ppublish
SO  - J Exp Med. 1992 Dec 1;176(6):1489-95. doi: 10.1084/jem.176.6.1489.