PMID- 28317464
OWN - NLM
STAT- MEDLINE
DCOM- 20171228
LR  - 20180206
IS  - 1091-7691 (Electronic)
IS  - 0895-8378 (Linking)
VI  - 29
IP  - 2
DP  - 2017 Feb
TI  - Molecular mechanisms of pulmonary response progression in crystalline silica 
      exposed rats.
PG  - 53-64
LID - 10.1080/08958378.2017.1282064 [doi]
AB  - An understanding of the mechanisms underlying diseases is critical for their 
      prevention. Excessive exposure to crystalline silica is a risk factor for 
      silicosis, a potentially fatal pulmonary disease. Male Fischer 344 rats were 
      exposed by inhalation to crystalline silica (15 mg/m(3), six hours/day, five 
      days) and pulmonary response was determined at 44 weeks following termination of 
      silica exposure. Additionally, global gene expression profiling in lungs and BAL 
      cells and bioinformatic analysis of the gene expression data were done to 
      understand the molecular mechanisms underlying the progression of pulmonary 
      response to silica. A significant increase in lactate dehydrogenase activity and 
      albumin content in BAL fluid (BALF) suggested silica-induced pulmonary toxicity 
      in the rats. A significant increase in the number of alveolar macrophages and 
      infiltrating neutrophils in the lungs and elevation in monocyte chemoattractant 
      protein-1 (MCP-1) in BALF suggested the induction of pulmonary inflammation in 
      the silica exposed rats. Histological changes in the lungs included granuloma 
      formation, type II pneumocyte hyperplasia, thickening of alveolar septa and 
      positive response to Masson's trichrome stain. Microarray analysis of global gene 
      expression detected 94 and 225 significantly differentially expressed genes in 
      the lungs and BAL cells, respectively. Bioinformatic analysis of the gene 
      expression data identified significant enrichment of several disease and 
      biological function categories and canonical pathways related to pulmonary 
      toxicity, especially inflammation. Taken together, these data suggested the 
      involvement of chronic inflammation as a mechanism underlying the progression of 
      pulmonary response to exposure of rats to crystalline silica at 44 weeks 
      following termination of exposure.
FAU - Sellamuthu, Rajendran
AU  - Sellamuthu R
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - Umbright, Christina
AU  - Umbright C
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - Roberts, Jenny R
AU  - Roberts JR
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - Young, Shih-Houng
AU  - Young SH
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - Richardson, Diana
AU  - Richardson D
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - McKinney, Walter
AU  - McKinney W
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - Chen, Bean T
AU  - Chen BT
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - Li, Shengqiao
AU  - Li S
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - Kashon, Michael
AU  - Kashon M
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
FAU - Joseph, Pius
AU  - Joseph P
AD  - a Health Effects Laboratory Division , National Institute for Occupational Safety 
      and Health (NIOSH) , Morgantown , WV , USA.
LA  - eng
PT  - Journal Article
DEP - 20170319
PL  - England
TA  - Inhal Toxicol
JT  - Inhalation toxicology
JID - 8910739
RN  - 7631-86-9 (Silicon Dioxide)
SB  - IM
MH  - Animals
MH  - Bronchoalveolar Lavage Fluid/chemistry/cytology/immunology
MH  - Cell Count
MH  - Gene Expression Profiling
MH  - Lung/*drug effects/immunology/metabolism/pathology
MH  - Macrophages/immunology
MH  - Male
MH  - Rats
MH  - Rats, Inbred F344
MH  - Silicon Dioxide/*toxicity
OTO - NOTNLM
OT  - Crystalline silica
OT  - gene expression profile
OT  - pulmonary toxicity
OT  - toxicity mechanisms
EDAT- 2017/03/21 06:00
MHDA- 2017/12/29 06:00
CRDT- 2017/03/21 06:00
PHST- 2017/03/21 06:00 [pubmed]
PHST- 2017/12/29 06:00 [medline]
PHST- 2017/03/21 06:00 [entrez]
AID - 10.1080/08958378.2017.1282064 [doi]
PST - ppublish
SO  - Inhal Toxicol. 2017 Feb;29(2):53-64. doi: 10.1080/08958378.2017.1282064. Epub 
      2017 Mar 19.