PMID- 9458799
OWN - NLM
STAT- MEDLINE
DCOM- 19980219
LR  - 20190509
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 274
IP  - 1
DP  - 1998 Jan
TI  - Chemokine regulation of ozone-induced neutrophil and monocyte inflammation.
PG  - L39-46
LID - 10.1152/ajplung.1998.274.1.L39 [doi]
AB  - Pulmonary inflammation has been observed in humans and in many animal species 
      after ozone exposure. Inflammatory cell accumulation involves local synthesis of 
      chemokines, including neutrophil chemoattractants such as macrophage inflammatory 
      protein-2 (MIP-2), and monocyte chemoattractants, such as monocyte 
      chemoattractant protein-1 (MCP-1). To better understand the mechanism of 
      ozone-induced inflammation, we exposed mice and rats to ozone for 3 h and 
      measured MIP-2 and MCP-1 gene expression. In C57BL/6 mice, steady-state mRNA 
      levels for MCP-1 in the lung increased at 0.6 parts/million (ppm) ozone and were 
      maximal at 2.0 ppm ozone. After exposure to 2 ppm ozone, MIP-2 mRNA levels peaked 
      at 4 h postexposure, whereas MCP-1 mRNA levels peaked at 24 h postexposure. 
      Neutrophils and monocytes recovered in bronchoalveolar lavage fluid peaked at 24 
      and 72 h, respectively. The accumulation of monocytes was thus delayed relative 
      to that of neutrophils, consistent with the sequential expression of the 
      corresponding chemokines. The role of MCP-1 in monocyte accumulation was 
      evaluated in greater detail in rats. Ozone caused an increase in monocyte 
      chemotactic activity in bronchoalveolar fluid that was inhibited by an antibody 
      directed against MCP-1. Ozone-induced MCP-1 mRNA levels were higher in lavage 
      cells than in whole lung tissue, indicating that lavage cells are an important 
      source of MCP-1. In these cells, nuclear factor-kappa B, a nuclear transcription 
      factor implicated in MCP-1 gene regulation, was also activated 20-24 h after 
      ozone exposure. These findings indicate that monocyte accumulation subsequent to 
      acute lung injury can be mediated through MCP-1 and that nuclear factor-kappa B 
      may play a role in ozone-induced MCP-1 gene expression.
FAU - Zhao, Q
AU  - Zhao Q
AD  - Department of Environmental Health, University of Cincinnati 45267, USA.
FAU - Simpson, L G
AU  - Simpson LG
FAU - Driscoll, K E
AU  - Driscoll KE
FAU - Leikauf, G D
AU  - Leikauf GD
LA  - eng
GR  - P30-ES-06096/ES/NIEHS NIH HHS/United States
GR  - R01-ES-06562/ES/NIEHS NIH HHS/United States
GR  - R01-ES-06677/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Chemotactic Factors)
RN  - 0 (DNA Primers)
RN  - 0 (Monokines)
RN  - 0 (Nuclear Proteins)
RN  - 0 (RNA, Messenger)
RN  - 66H7ZZK23N (Ozone)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/chemistry/cytology
MH  - Chemokine CCL2/*biosynthesis
MH  - Chemokine CXCL2
MH  - Chemotactic Factors/biosynthesis
MH  - Chemotaxis, Leukocyte/*drug effects/physiology
MH  - DNA Primers
MH  - Gene Expression Regulation/*drug effects/physiology
MH  - Inflammation/chemically induced/*physiopathology
MH  - Kinetics
MH  - Lung/drug effects/physiology/*physiopathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Monocytes/drug effects/*physiology
MH  - Monokines/*biosynthesis
MH  - Neutrophils/drug effects/*physiology
MH  - Nuclear Proteins/isolation & purification/metabolism
MH  - Ozone/*toxicity
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Rats, Wistar
MH  - Transcription, Genetic/drug effects
EDAT- 1998/02/12 00:00
MHDA- 1998/02/12 00:01
CRDT- 1998/02/12 00:00
PHST- 1998/02/12 00:00 [pubmed]
PHST- 1998/02/12 00:01 [medline]
PHST- 1998/02/12 00:00 [entrez]
AID - 10.1152/ajplung.1998.274.1.L39 [doi]
PST - ppublish
SO  - Am J Physiol. 1998 Jan;274(1):L39-46. doi: 10.1152/ajplung.1998.274.1.L39.