TY - JOUR
T1 - Urban air pollution produces up-regulation of myocardial inflammatory genes and dark chocolate provides cardioprotection
AU - Villarreal-Calderon, Rodolfo
AU - Reed, William
AU - Palacios-Moreno, Juan
AU - Keefe, Sheyla
AU - Herritt, Lou
AU - Brooks, Diane
AU - Torres-Jardón, Ricardo
AU - Calderón-Garcidueñas, Lilian
N1 - Funding Information:
We deeply appreciate Dr. Robert R. Maronpot's critical review of the paper and the technical support of Norma Osnaya and Silvia Monroy from the INP. This work was supported in part by the NCRR Grant # P20RRO15583 and was presented in part at the 7th European Congress of Toxicological Pathology on September 16–18, 2009, in The Hague, The Netherlands as well as at the 2009 American Thoracic Society International Conference in San Diego, CA, by Rodolfo Villarreal-Calderon who received an ATS Minority Trainee Travel Award therein.
PY - 2012/5
Y1 - 2012/5
N2 - Air pollution is a serious environmental problem. Elderly subjects show increased cardiac morbidity and mortality associated with air pollution exposure. Mexico City (MC) residents are chronically exposed to high concentrations of fine particulate matter (PM 2.5) and PM-associated lipopolysaccharides (PM-LPS). To test the hypothesis that chronic exposure to urban pollution produces myocardial inflammation, female Balb-c mice age 4 weeks were exposed for 16 months to two distinctly different polluted areas within MC: southwest (SW) and northwest (NW). SW mice were given either no treatment or chocolate 2g/9.5mg polyphenols/3 times per week. Results were compared to mice kept in clean air. Key inflammatory mediator genes: cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and the LPS receptor CD14 (cluster of differentiation antigen 14) were measured by real-time polymerase chain reaction. Also explored were target NFκB (nuclear factor κB), oxidative stress and antioxidant defense genes.TNF-α, IL-6, and COX-2 were significantly increased in both NW and SWMC mice (p=. 0.0001). CD14 was up-regulated in SW mice in keeping with the high exposures to particulate matter associated endotoxin. Chocolate administration resulted in a significant down-regulation of TNF-α (p<. 0.0001), IL-6 (p=. 0.01), and IL-1β (p=. 0.02). The up-regulation of antioxidant enzymes and the down-regulation of potent oxidases, toll-like receptors, and pro-apoptotic signaling genes completed the protective profile.Exposure to air pollution produces up-regulation of inflammatory myocardial genes and endotoxin plays a key role in the inflammatory response. Regular consumption of dark chocolate may reduce myocardial inflammation and have cardioprotective properties in the setting of air pollution exposures.
AB - Air pollution is a serious environmental problem. Elderly subjects show increased cardiac morbidity and mortality associated with air pollution exposure. Mexico City (MC) residents are chronically exposed to high concentrations of fine particulate matter (PM 2.5) and PM-associated lipopolysaccharides (PM-LPS). To test the hypothesis that chronic exposure to urban pollution produces myocardial inflammation, female Balb-c mice age 4 weeks were exposed for 16 months to two distinctly different polluted areas within MC: southwest (SW) and northwest (NW). SW mice were given either no treatment or chocolate 2g/9.5mg polyphenols/3 times per week. Results were compared to mice kept in clean air. Key inflammatory mediator genes: cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), and the LPS receptor CD14 (cluster of differentiation antigen 14) were measured by real-time polymerase chain reaction. Also explored were target NFκB (nuclear factor κB), oxidative stress and antioxidant defense genes.TNF-α, IL-6, and COX-2 were significantly increased in both NW and SWMC mice (p=. 0.0001). CD14 was up-regulated in SW mice in keeping with the high exposures to particulate matter associated endotoxin. Chocolate administration resulted in a significant down-regulation of TNF-α (p<. 0.0001), IL-6 (p=. 0.01), and IL-1β (p=. 0.02). The up-regulation of antioxidant enzymes and the down-regulation of potent oxidases, toll-like receptors, and pro-apoptotic signaling genes completed the protective profile.Exposure to air pollution produces up-regulation of inflammatory myocardial genes and endotoxin plays a key role in the inflammatory response. Regular consumption of dark chocolate may reduce myocardial inflammation and have cardioprotective properties in the setting of air pollution exposures.
KW - Air pollution
KW - CD14
KW - Cardioprotection
KW - Dark chocolate
KW - Endotoxin
KW - IL-1β
KW - IL-6
KW - Myocardial inflammation
KW - Particulate matter
KW - TNF-α
UR - http://www.scopus.com/inward/record.url?scp=84859426029&partnerID=8YFLogxK
U2 - 10.1016/j.etp.2010.09.002
DO - 10.1016/j.etp.2010.09.002
M3 - Article
C2 - 20932730
AN - SCOPUS:84859426029
SN - 0940-2993
VL - 64
SP - 297
EP - 306
JO - Experimental and Toxicologic Pathology
JF - Experimental and Toxicologic Pathology
IS - 4
ER -