PMID- 8929547
OWN - NLM
STAT- MEDLINE
DCOM- 19961223
LR  - 20190516
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 60
IP  - 5
DP  - 1996 Nov
TI  - C-C chemokine-induced eosinophil chemotaxis during allergic airway inflammation.
PG  - 573-8
AB  - The production of eosinophil-specific chemotactic factors during allergic airway 
      responses may be a pivotal event resulting in eosinophil accumulation, 
      activation, and airway damage. Recent studies have identified specific chemokines 
      that may play crucial roles in recruitment of eosinophils to the site of allergic 
      reactions. In this study we have utilized an established model of schistosome egg 
      antigen (SEA) -mediated allergic responses to examine the role of specific C-C 
      chemokines [macrophage inflammatory protein-1alpha (MIP-1alpha), RANTES, and 
      monocyte chemoattractant protein-1 (MCP-1)] in eosinophil recruitment. We have 
      previously identified a role for MIP-1alpha in eosinophil accumulation in the 
      lung and airway during allergic airway inflammation. We extend those studies 
      using in vitro eosinophil chemotaxis to establish that both MIP-1alpha and RANTES 
      are potent eosinophil chemotactic factors in lungs during allergic airway 
      responses. Morphometric analysis demonstrated a peribronchial accumulation of 
      eosinophils within the lungs beginning at 8 h, peaking at 24 h, and plateauing at 
      48-96 h after allergen (SEA) challenge. Utilizing whole-lung homogenates from 
      allergen-challenged mice, in vitro eosinophil chemotactic assays demonstrated 
      significant increases in eosinophil chemotactic activity with 8-h lung 
      homogenates and peak activity with samples from 24-h lung homogenates. These data 
      correlated with the morphometric analysis of peribronchial eosinophil 
      accumulation in situ. When lung homogenates from allergen-challenged mice were 
      preincubated in vitro with antibodies specific for MIP-1alpha, RANTES, or MCP-1, 
      a significant reduction in eosinophil chemotaxis was observed with only 
      MIP-1alpha and RANTES neutralization. Altogether, these studies indicate that 
      RANTES and MIP-1alpha are major eosinophil chemotactic factors produced during 
      allergic airway responses.
FAU - Lukacs, N W
AU  - Lukacs NW
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor 
      48109-0602, USA.
FAU - Standiford, T J
AU  - Standiford TJ
FAU - Chensue, S W
AU  - Chensue SW
FAU - Kunkel, R G
AU  - Kunkel RG
FAU - Strieter, R M
AU  - Strieter RM
FAU - Kunkel, S L
AU  - Kunkel SL
LA  - eng
GR  - AI36302/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Allergens)
RN  - 0 (Antibodies)
RN  - 0 (Antigens, Helminth)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Macrophage Inflammatory Proteins)
SB  - IM
MH  - Allergens/immunology/toxicity
MH  - Alveolitis, Extrinsic Allergic/etiology/immunology/*physiopathology
MH  - Animals
MH  - Antibodies/pharmacology
MH  - Antigens, Helminth/immunology/toxicity
MH  - Asthma/immunology/*physiopathology
MH  - Cells, Cultured
MH  - Chemokine CCL2/antagonists & inhibitors/*pharmacology
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemokine CCL5/antagonists & inhibitors/*pharmacology
MH  - Chemotaxis, Leukocyte/*drug effects
MH  - Eosinophils/*drug effects
MH  - Female
MH  - Immunization
MH  - Macrophage Inflammatory Proteins/antagonists & inhibitors/*pharmacology
MH  - Mice
MH  - Mice, Inbred CBA
MH  - Rabbits
MH  - Schistosoma mansoni/immunology
MH  - Specific Pathogen-Free Organisms
MH  - Th2 Cells/immunology
EDAT- 1996/11/01 00:00
MHDA- 1996/11/01 00:01
CRDT- 1996/11/01 00:00
PHST- 1996/11/01 00:00 [pubmed]
PHST- 1996/11/01 00:01 [medline]
PHST- 1996/11/01 00:00 [entrez]
AID - 10.1002/jlb.60.5.573 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1996 Nov;60(5):573-8. doi: 10.1002/jlb.60.5.573.