African Dust Storms Reaching Puerto Rican Coast Stimulate the Secretion of IL-6 and IL-8 and Cause Cytotoxicity to Human Bronchial Epithelial Cells (BEAS-2B)

作     者：Rosa I. Rodríguez-Cotto Mario G. Ortiz-Martínez Evasomary Rivera-Ramírez Loyda B. Méndez Julio C. Dávila Braulio D. Jiménez-Vélez 

作者机构：Department of Biochemistry University of Puerto Rico-Medical Sciences Campus San Juan Puerto Rico Center for Environmental and Toxicological Research San Juan Puerto Rico Department of Biochemistry University of Puerto Rico-Medical Sciences Campus San Juan Puerto Rico Center for Environmental and Toxicological Research San Juan Puerto Rico Science and Technology School Eastern University Carolina Puerto Rico Department of Biochemistry University of Puerto Rico-Medical Sciences Campus San Juan Puerto Rico Center for Environmental and Toxicological Research San Juan Puerto Rico 

出 版 物：《Health》 (健康（英文）)

年 卷 期：2013年第5卷第10期

页      面：14-28页

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主　　题：Dust Storm Particulate Matter Endotoxins Metals BEAS-2B Cells 

摘      要：African dust storm events (ADE) travel across theAtlantic Ocean(ADEAO) and reach the Puerto Rican coast (ADEPRC), potentially impacting air quality and human health. To what extent seasonal variations in atmospheric particulate matter (PM) size fractions, composition and sources trigger respiratory-adverse effects to Puerto Ricans is still unclear. In the present study, we investigated the pro-inflammatory and cytotoxic effects of PM samples harvested during ADEAO (PM10), ADEPRC (PM2.5 and PM10) and Non-ADE (Pre-and Post-ADEAO and Non-ADEPRC), using BEAS-2B cells. Endotoxins (ENX) in PM2.5 and PM10 extracts and traces of metals (TMET) in PM2.5 extracts were also examined. IL-6 and IL-8 secretion and cytotoxicity were used as endpoints. ADEAO and ADEPRC extracts were found to be more cytotoxic than Non-ADE and ADEAO were more toxic than ADEPRC extracts. PM10 extracts from ADEAO and Post-ADEAO caused significant secretion of IL-8. IL-6 and IL-8 secretion was higher following treatment with PM10 and PM2.5 ADEPRC than with Non-ADEPRC extracts. ENX levels were found to be higher in PM10 ADEAO than in the rest of the samples tested. TMET levels were higher in PM2.5 ADEPRC than in Non-ADEPRC extracts. Deferoxamine significantly reduced cytotoxicity and IL-6 and IL-8 secretion whereas Polymyxin B did not. TMET in PM2.5 fractions is a major determinant in ADEPRC-induced toxicity and work in conjunction with ENX to cause toxicity to lung cells in vitro. ENX and TMET may be responsible, in part, for triggering PM-respiratory adverse responses in susceptible and predisposed individuals.