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Ambient Particulate Matter Induces lnterleukin-8 Expression through an Alternative NF-κB (Nuclear Factor-Kappa B) Mechanism in Human Airway Epithelial Cells

Background: Exposure to ambient air paniculate matter (PM) has been shown to increase rates of cardiopulmonary morbidity and mortality, but the underlying mechanisms are still not well understood. Objective: We examined signaling events involved in the expression of the inflammatory gene... Full description

1st Person: Silbajoris, Robert
Additional Persons: Osornio-Vargas, Alvaro R. verfasserin; Simmons, Steven O. verfasserin; Reed, William verfasserin; Bromberg, Philip A. verfasserin; Dailey, Lisa A. verfasserin; Samet, James M. verfasserin
Source: in Environmental health perspectives : EHP Vol. 119, No. 10 (2011), p. 1379-1383
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Type of Publication: Article
Language: English
Published: 2011
Keywords: research-article
Online: Volltext
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100 1 |a Silbajoris, Robert 
245 1 0 |a Ambient Particulate Matter Induces lnterleukin-8 Expression through an Alternative NF-κB (Nuclear Factor-Kappa B) Mechanism in Human Airway Epithelial Cells  |h Elektronische Ressource 
300 |a Online-Ressource 
520 |a Background: Exposure to ambient air paniculate matter (PM) has been shown to increase rates of cardiopulmonary morbidity and mortality, but the underlying mechanisms are still not well understood. Objective: We examined signaling events involved in the expression of the inflammatory gene interleukin-8 (IL-8) in human airway epithelial cells (HAECs) exposed to ambient PM collected in an urban area of Mexicali, Mexico. Methods: We studied IL-8 expression and regulatory signaling pathways in cultured HAECs exposed to Mexicali PM suspended in media for 0—4 hr. Results: Exposure resulted in a dose-dependent, 2- to 8-fold increase in IL-8 mRNA expression relative to controls. PM exposure induced IL-8 transcriptional activity in BEAS-2B cells that was dependent on the nuclear factor-kappa B (NF-κB) response element in the IL-8 promoter. Chromatin immunoprecipitation (ChIP) assays showed a 3-fold increase in binding of the p65 (RelA) (NF-κB) isoform to the IL-8 promoter sequence in HAECs exposed to PM. Western blot analyses showed elevated levels of phosphorylation of p65 but no changes in IκBα phosphorylation or degradation. IL-8 expression was blunted in a dose-dependent manner in BEAS-2B cells transduced with a lentivirus encoding a dominant negative p65 mutant in which phosphorylation sites were inactivated. Conclusion: Taken together, these findings show that the increase in IL-8 mRNA expression in HAECs exposed to PM₁₀ (PM ≤ 10 μm in aerodynamic diameter) is mediated through an NF-κB-dependent signaling mechanism that occurs through a pathway involving direct phosphorylation of the transcription factor p65 in the absence of IκBα degradation. These data show that exposure to PM₁₀ in ambient air can induce inflammatory responses by activating specific signaling mechanisms in HAECs. 
653 |a research-article 
700 1 |a Osornio-Vargas, Alvaro R.  |e verfasserin  |4 aut 
700 1 |a Simmons, Steven O.  |e verfasserin  |4 aut 
700 1 |a Reed, William  |e verfasserin  |4 aut 
700 1 |a Bromberg, Philip A.  |e verfasserin  |4 aut 
700 1 |a Dailey, Lisa A.  |e verfasserin  |4 aut 
700 1 |a Samet, James M.  |e verfasserin  |4 aut 
773 0 8 |i in  |t Environmental health perspectives : EHP  |d Research Triangle Park, N.C. [u.a.]  |g Vol. 119, No. 10 (2011), p. 1379-1383  |q 119:10<1379-1383  |w (DE-601)JST031217095  |x 0091-6765 
856 4 1 |u https://www.jstor.org/stable/41263047  |3 Volltext 
912 |a GBV_JSTOR 
951 |a AR 
952 |d 119  |j 2011  |e 10  |h 1379-1383 

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