Chonnam Med J.  2008 Apr;44(1):1-9. 10.4068/cmj.2008.44.1.1.

Particulate Air Pollutants and Airway Inflammation

• Jang AS
• Park CS
• Choi IS

• KMID: 1973383
• DOI: http://doi.org/10.4068/cmj.2008.44.1.1

Abstract

Particulate air pollutants emanating from traffic and various industries are related to allergic airway disorders including asthma. Particulate air pollutants inhalation directly induces lung inflammation to allergens or respiratory viral infection as an adjuvant by macrophages and epithelial cells. Inhalation of particulate air pollutants aggravates respiratory symptoms in patients with chronic airway diseases, but the mechanisms underlying this response remain poorly understood. Diesel exhaust particles induced airway hyperresponsiveness and Ym mRNA expression via a Th2 cell-biased response, which synthesized by activated macrophages are homologous to chitinase and have chitinase activity. Alveolar macrophages play an important role in particles-induced airway and lung inflammation via direct production of IL-13. Treatment of epithelial cells with bovine serum albumin coated titanium dioxide particles altered 20 protein spots on the two-dimensional gel, and these were then analyzed by nano-LC-MS/MS. These proteins included defense-related, cell-activating, and cytoskeletal proteins implicated in the response to oxidative stress. TiO2 treatment was found to increase the amount of mRNA for macrophage migration-inhibitory factor (MIF). MIF was expressed primarily in epithelium and was elevated in lung tissues and bronchoalveolar lavage fluids of TiO2-treated rats as compared with sham treated rats. Carbon black and diesel exhaust particles also induced expression of MIF protein in the epithelial cells. We attempt to offer insight into how particles may influence airway inflammation.

Keyword

Air pollution; Lung; Inflammation

MeSH Terms

Air Pollution
Allergens
Animals
Asthma
Bronchoalveolar Lavage Fluid
Chitinase
Cytoskeletal Proteins
Epithelial Cells
Epithelium
Humans
Inflammation
Inhalation
Interleukin-13
Lung
Macrophages
Macrophages, Alveolar
Oxidative Stress
Particulate Matter
Pneumonia
Proteins
Rats
RNA, Messenger
Salicylamides
Serum Albumin, Bovine
Soot
Titanium
Vehicle Emissions
Allergens
Chitinase
Cytoskeletal Proteins
Interleukin-13
Particulate Matter
Proteins
RNA, Messenger
Salicylamides
Serum Albumin, Bovine
Soot
Titanium
Vehicle Emissions

Figure

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  Fig. 1. The expression of Ym1 and YM2 mRNA in the lungs of DEP-treated and control mice. Lung tissues from DEP-treated and control mice were stained with monoclonal antibodies directed against YM1 and YM2.

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  Fig. 2. MR angiography with Gadolinium demonstrates complete occlusion of right distal ICA, right MCA and right ACA.

• 

  Fig. 3. Time and dose responses of IL-13 production by macrophages exposed to TiO2 particles. Purified alveolar macrophages stimulated with 1, 10, and 40μg/ml TiO2 for 24, 48, and 72 hours (n=6 in each experiment). The control group (n=6) consisted of unstimulated alveolar macrophages. The IL-13 in the 48-hour culture supernatants is produced in a dose-dependent manner following TiO2 treatment (A). TiO2 concentrations higher than 10μg/ml significantly enhance IL-13 production when compared with the control group. The production of IL-13 protein is increased in a time-dependent manner and peaks 48 hours after TiO2 stimulation (B). The results are expressed as means±SEM.

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  Fig. 4. Cluster analysis of 20 proteins with significant differential expression (>2-fold change) at 8 or 48 h caused by TiO2 treatment of BEAS-2B epithelial cells. The expression profiles of the individual proteins were classified by cluster analysis. Protein names (National Center for Biotechnology Information (NCBI)) are displayed for each cluster.

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  Fig. 5. Semiquantitative RT-PCR analysis of TALDO1, CLIC1, and MIF mRNA expression. The levels of mRNA for TALDO1, CLIC1, and MIF were estimated in extracts of BEAS-2B cells stimulated with TiO2 particles (20 μg/105 cells). Expression levels were determined by densitometry and normalized to the level of GAPDH mRNA.

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