US EPA

5068907 

Journal Article 

Abstract 

The association of vanadium pentoxide and inflammatory response in patients with copd and in human bronchial epithelial cell 

Lin, SH; Lin, CH; Li, YR; Ching, YY; Chang, HH 

2018 

1 

Respirology
ISSN: 1323-7799
EISSN: 1440-1843 

23 

Supplement 2 

109, AP052 

English 

10.1111/resp.13420_51 

WOS:000456217200272 

Background and Aims
Chronic obstructive pulmonary disease (COPD) is characterized by lung inflammation. Air pollution is strongly related to chronic obstructive pulmonary disease (COPD). Vanadium (V) is major transition metal often adhered to particulate matter and emitted into the atmosphere as vanadium pentoxide (V2O5) by the combustion of fossil fuels and metallurgic industry activities. Particulate matter (PM) air pollution contributes to inflammation‐related processes including COPD. Our aim is to evaluate the effect of vanadium on the inflammatory response in vitro and in patients with COPD.

Methods
The expression of proinflammatory cytokine and chemokine mRNA analyzed by real‐time PCR. Reactive oxygen species (ROS) level determined by flow cytometry using DCF‐DA staining. Cytometric bead‐based assays were used to quantify inflammatory cytokines in the culture media and the plasma of healthy and COPD subjects. p‐ERK and p‐JNK expression were performed by western blot. Statistical analyses were performed using unpaired t‐test at P < 0.05 with GraphPad Prism version.

Results
Our finding identified a positive relationship between the concentration of vanadium in urine and the expression of inflammatory factor (IL‐8, MCP‐1) in plasma of patients with COPD. Moreover, V2O5 induces IL‐8, MCP‐1, IP‐10 and CXCL‐11 mRNA expression and increase ROS production in BEAS‐2B human bronchial epithelial cell. Treatment with N‐acetylcysteine protects against V2O5‐stimulated ROS production and down‐regulation of IL‐8, MCP‐1, IP‐10 and CXCL‐11 mRNA expression in BEAS‐2B cells. MAPK pathways are typically involved in inflammation. V2O5 treatment increase p‐ERK and p‐JNK expression in BEAS‐2B stimulated with V2O5.

Conclusion
Our finding demonstrate that inflammatory response in patient with COPD is associated with vanadium, a usually component of particulate matter. And V2O5 induce excessive inflammation through activating MAPK mediated oxidative stress signalling in BEAS‐2B human bronchial epithelial cell. These evidence show that vanadium and its oxidant may contribute to chronic inflammation in patient with COPD. 

23rd Congress of the Asian Pacific Society of Respirology 

Taipei, Taiwan 

29 November–2 December 2018