PMID- 12588706
OWN - NLM
STAT- MEDLINE
DCOM- 20040326
LR  - 20200930
IS  - 1040-0605 (Print)
IS  - 1040-0605 (Linking)
VI  - 286
IP  - 3
DP  - 2004 Mar
TI  - Antimacrophage chemokine treatment prevents neutrophil and macrophage influx in 
      hyperoxia-exposed newborn rat lung.
PG  - L488-93
AB  - Macrophage-derived cytokines may provoke the inflammatory response in lung 
      injury. Because macrophage influx is a prominent feature of the cellular 
      inflammatory response accompanying the development of bronchopulmonary dysplasia, 
      we hypothesized that blocking macrophage influx would reduce overall cellular 
      influx and oxidative damage. Newborn rats were exposed at birth to 95% O(2) or 
      air for 1 wk, and hyperoxia-exposed pups were injected with anti-monocyte 
      chemoattractant protein-1 (MCP-1) or IgG control on days 3-5. MCP-1 was increased 
      in bronchoalveolar lavage fluid and in histological sections from the 95% 
      O(2)-exposed, IgG-injected pups compared with air-exposed controls. At 1 wk, 
      anti-MCP-1-treated pups had reduced leukocyte numbers, both macrophages and 
      neutrophils, in bronchoalveolar lavage fluid compared with IgG-treated controls. 
      Cytokine-induced neutrophil chemoattractant-1, the rat analog of IL-8, was not 
      significantly decreased in lavage fluid but was reduced in lung cells in 
      anti-MCP-1-treated pups. Tissue carbonyls, a measure of protein oxidation, were 
      decreased in anti-MCP-1-treated pups. Anti-MCP-1 treatment prevented neutrophil 
      influx and reduced protein oxidation in hyperoxia-exposed newborn rats.
FAU - Vozzelli, Michael A
AU  - Vozzelli MA
AD  - Department of Pediatrics, Division of Neonatal Medicine, Neonatal-Perinatal 
      Research Institute, Durham, NC 27710, USA. auten@duke.edu
FAU - Mason, S Nicholas
AU  - Mason SN
FAU - Whorton, Mary H
AU  - Whorton MH
FAU - Auten, Richard L Jr
AU  - Auten RL Jr
LA  - eng
GR  - HL-67021/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20030214
PL  - United States
TA  - Am J Physiol Lung Cell Mol Physiol
JT  - American journal of physiology. Lung cellular and molecular physiology
JID - 100901229
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 7440-44-0 (Carbon)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Bronchoalveolar Lavage Fluid/cytology/immunology
MH  - Bronchopulmonary Dysplasia/*immunology
MH  - Carbon/metabolism
MH  - Chemokine CCL2/metabolism/pharmacology
MH  - Chemokines, CXC/metabolism
MH  - Female
MH  - Humans
MH  - Hyperoxia/immunology
MH  - Hypoxia/*immunology
MH  - Infant, Newborn
MH  - Intercellular Signaling Peptides and Proteins/metabolism
MH  - Lung/cytology/*immunology/metabolism
MH  - Macrophages/*cytology/immunology
MH  - Neutrophils/*cytology/immunology
MH  - Oxidative Stress/immunology
MH  - Pregnancy
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Respiratory Mucosa/cytology/immunology/metabolism
EDAT- 2003/02/18 04:00
MHDA- 2004/03/27 05:00
CRDT- 2003/02/18 04:00
PHST- 2003/02/18 04:00 [pubmed]
PHST- 2004/03/27 05:00 [medline]
PHST- 2003/02/18 04:00 [entrez]
AID - 00414.2002 [pii]
AID - 10.1152/ajplung.00414.2002 [doi]
PST - ppublish
SO  - Am J Physiol Lung Cell Mol Physiol. 2004 Mar;286(3):L488-93. doi: 
      10.1152/ajplung.00414.2002. Epub 2003 Feb 14.