PMID- 15866772
OWN - NLM
STAT- MEDLINE
DCOM- 20050816
LR  - 20181113
IS  - 0091-6765 (Print)
IS  - 1552-9924 (Electronic)
IS  - 0091-6765 (Linking)
VI  - 113
IP  - 5
DP  - 2005 May
TI  - Time course of gene expression of inflammatory mediators in rat lung after diesel 
      exhaust particle exposure.
PG  - 612-7
AB  - Diesel exhaust particles (DEPs) at three concentrations (5, 35, and 50 mg/kg body 
      weight) were instilled into rats intratracheally. We studied gene expression at 
      1, 7, and 30 days postexposure in cells obtained by bronchoalveolar lavage (BAL) 
      and in lung tissue. Using real-time reverse transcriptase-polymerase chain 
      reaction (RT-PCR), we measured the mRNA levels of eight genes [interleukin 
      (IL)-1beta, IL-6, IL-10, iNOS (inducible nitric oxide synthase), MCP-1 (monocyte 
      chemoattractant protein-1), MIP-2 (macrophage inflammatory protein-2), TGF-beta1 
      (transforming growth factor-beta1), and TNF-alpha (tumor necrosis factor-alpha )] 
      in BAL cells and four genes [IL-6, ICAM-1 (intercellular adhesion molecule-1), 
      GM-CSF (granulocyte/macrophage-colony stimulating factor), and RANTES (regulated 
      upon activation normal T cell expressed and secreted)] in lung tissue. In BAL 
      cells on day 1, high-dose exposure induced a significant up-regulation of 
      IL-1beta, iNOS, MCP-1, and MIP-2 but no change in IL-6, IL-10, TGF-beta1, and 
      TNF-alpha mRNA levels. There was no change in the mRNA levels of IL-6, RANTES, 
      ICAM-1, and GM-CSF in lung tissue. Nitric oxide production and levels of MCP-1 
      and MIP-2 were increased in the 24-hr culture media of alveolar macrophages (AMs) 
      obtained on day 1. IL-6, MCP-1, and MIP-2 levels were also elevated in the BAL 
      fluid. BAL fluid also showed increases in albumin and lactate dehydrogenase. The 
      cellular content in BAL fluid increased at all doses and at all time periods, 
      mainly due to an increase in polymorphonuclear leukocytes. In vitro studies in 
      AMs and cultured lung fibroblasts showed that lung fibroblasts are a significant 
      source of IL-6 and MCP-1 in the lung.
FAU - Rao, K Murali Krishna
AU  - Rao KM
AD  - Pathology and Physiology Research Branch, Health Effects Laboratory Division, 
      National Institute for Occupational Safety and Health, 1095 Willowdale Road, 
      Morgantown, WV 26505, USA. mir8@cdc.gov
FAU - Ma, Jane Y C
AU  - Ma JY
FAU - Meighan, Terence
AU  - Meighan T
FAU - Barger, Mark W
AU  - Barger MW
FAU - Pack, Donna
AU  - Pack D
FAU - Vallyathan, Val
AU  - Vallyathan V
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Environ Health Perspect
JT  - Environmental health perspectives
JID - 0330411
RN  - 0 (Cytokines)
RN  - 0 (RNA, Messenger)
RN  - 0 (Vehicle Emissions)
RN  - 31C4KY9ESH (Nitric Oxide)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/immunology
MH  - Cell Culture Techniques
MH  - Cytokines/*biosynthesis/immunology
MH  - Fibroblasts
MH  - *Gene Expression Profiling
MH  - *Inflammation
MH  - Lung Diseases/*etiology/immunology
MH  - Macrophages, Alveolar/immunology
MH  - Nitric Oxide/analysis
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Time Factors
MH  - Vehicle Emissions/*adverse effects
PMC - PMC1257556
EDAT- 2005/05/04 09:00
MHDA- 2005/08/17 09:00
PMCR- 2005/05/01
CRDT- 2005/05/04 09:00
PHST- 2005/05/04 09:00 [pubmed]
PHST- 2005/08/17 09:00 [medline]
PHST- 2005/05/04 09:00 [entrez]
PHST- 2005/05/01 00:00 [pmc-release]
AID - ehp0113-000612 [pii]
AID - 10.1289/ehp.7696 [doi]
PST - ppublish
SO  - Environ Health Perspect. 2005 May;113(5):612-7. doi: 10.1289/ehp.7696.