Kinetic analysis of cytokine response to cigarette smoke condensate by human endothelial and monocytic cells

Nordskog, Brian K.; Fields, Wanda; Hellmann, Gary M.

doi:10.1016/j.tox.2005.04.005

Cited by 38 publications

(40 citation statements)

References 27 publications

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“…2011) and MCP‐1 (Nordskog et al. 2005) secretion decreased in macrophages exposed to cigarette smoke.…”

Section: Discussionmentioning

confidence: 91%

“…IL‐8 secretion has previously been shown to be increased in macrophages exposed to cigarette smoke exposure (Nordskog et al. 2005; Walters et al. 2005; Yang et al.…”

Section: Discussionmentioning

confidence: 99%

“…2007) and those exposed to cigarette smoke (Nordskog et al. 2005; Birrell et al. 2008; Bozinovski et al.…”

Section: Discussionmentioning

confidence: 99%

“…2000; Nordskog et al. 2005; Birrell et al. 2008) as well as in cultured alveolar macrophages from smokers compared with nonsmokers (Brown et al.…”

Section: Discussionmentioning

confidence: 99%

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Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

et al. 2017

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E‐cigarettes are perceived as harmless; however, evidence of their safety is lacking. New data suggests E‐cigarettes discharge a range of compounds capable of physiological damage to users. We previously established that cigarette smoke caused defective alveolar macrophage phagocytosis. The present study compared the effect E‐cigarette of components; E‐liquid flavors, nicotine, vegetable glycerine, and propylene glycol on phagocytosis, proinflammatory cytokine secretion, and phagocytic recognition molecule expression using differentiated THP‐1 macrophages. Similar to CSE, phagocytosis of NTHi bacteria was significantly decreased by E‐liquid flavoring (11.65–15.75%) versus control (27.01%). Nicotine also decreased phagocytosis (15.26%). E‐liquid, nicotine, and E‐liquid+ nicotine reduced phagocytic recognition molecules; SR‐A1 and TLR‐2. IL‐8 secretion increased with flavor and nicotine, while TNF α, IL‐1β, IL‐6, MIP‐1α, MIP‐1β, and MCP‐1 decreased after exposure to most flavors and nicotine. PG, VG, or PG:VG mix also induced a decrease in MIP‐1α and MIP‐1β. We conclude that E‐cigarettes can cause macrophage phagocytic dysfunction, expression of phagocytic recognition receptors and cytokine secretion pathways. As such, E‐cigarettes should be treated with caution by users, especially those who are nonsmokers.

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“…2011) and MCP‐1 (Nordskog et al. 2005) secretion decreased in macrophages exposed to cigarette smoke.…”

Section: Discussionmentioning

confidence: 91%

“…IL‐8 secretion has previously been shown to be increased in macrophages exposed to cigarette smoke exposure (Nordskog et al. 2005; Walters et al. 2005; Yang et al.…”

Section: Discussionmentioning

confidence: 99%

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Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

et al. 2017

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“…Among these, cigarette smoke and altered hemodynamic stress are major risk factors related to vascular inflammation and disease [1][2][3][4][5][6]. In vitro effects of cigarette smoke on vascular endothelial cells include impaired endothelial cell survival [7], induction of apoptosis [8], increased expression of vascular cell adhesion molecule-1 (VCAM-1), enhanced leukocyte adhesion [9], and increased endothelial cell inflammation [10]. Hemodynamic shear stress can inhibit inflammatory gene expression by vascular endothelial cells [11] under physiologic blood flow conditions, and induce endothelial cell activation and apoptosis [12], as well as platelet activation [13] under altered blood flow conditions.…”

Section: Introductionmentioning

confidence: 99%

Regulated complement deposition on the surface of human endothelial cells: Effect of tobacco smoke and shear stress

Yin

Ghebrehiwet

Weksler

et al. 2008

Thrombosis Research

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Cigarette smoke and hemodynamic stress both contribute to vascular inflammation and associated atherosclerosis. We recently demonstrated direct activation of complement components C4 and C3 on human endothelial cells (EC). The present study was designed to explore complement activation on bone marrow microvascular endothelial cells (BMEC) and human umbilical vein endothelial cells (HUVEC) in response to endothelial cell injury by tobacco smoke extract, shear stress, or other known inflammatory and atherogenic mediators, lipopolysaccharide (LPS) and INF-γ. Following treatment, confluent EC monolayers were exposed to plasma (60 min, 37 °C), and cell surface deposition of stable complement derivatives C4d, iC3b and SC5b-9 was measured in situ using an ELISA approach. Consistent with previous results, moderate levels of C4d, iC3b and SC5b-9 deposition were observed on native EC monolayers exposed to human plasma. Tobacco smoke and shear stress enhanced EC C4d deposition. In contrast, LPS and INF-γ failed to affect EC mediated complement activation, despite evidence of EC activation illustrated by ICAM-1 expression. The combination of tobacco smoke and shear stress nearly doubled EC C4d expression. No increases in iC3b or SC5b-9 were noted, suggesting inhibition of classical and alternative pathway C3 convertase assembly or activity. Indeed, concomitantly increased surface expression of complement regulatory proteins CD35 (CR1) and CD55 was observed following EC exposure to tobacco smoke and shear stress. These results suggest that a balance between complement activation and regulation exists at the EC surface, and may impact vascular injury leading to thrombosis, arteriosclerosis, and atherogenesis.

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Infection of human primary hepatocytes with dengue virus serotype 2

Suksanpaisan

Cabrera-Hernandez

Smith

2007

Journal of Medical Virology

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While the impact of the dengue viruses on liver function is prominent as shown by hepatomegaly, liver enzyme abnormality, occasional fulminant hepatic failure and histological changes including hepatocellular necrosis, significant debate exists as to the possible involvement of the predominant cell type in the liver, hepatocytes, in the disease process. To address this issue purified human primary hepatocytes were exposed to dengue virus serotype 2 and the production of de novo viral progeny was established by standard plaque assay, RT-PCR and immunocytochemistry. To investigate the response of the primary hepatocytes to infection, the expression of a panel of 9 cytokine genes (IFN-beta, TRAIL, MCP-1, IL-6, IL-1beta, IL-8, MIP-1alpha, MIP-1beta, and RANTES) was semi-quantitatively investigated by RT-PCR and up-regulation of TRAIL, MIP-1alpha, IFN-beta, MIP-1beta, IL-8, and RANTES was observed in response to infection. The induction of IL-8 in response to infection was accompanied by the secretion of IL-8 as verified by ELISA assay. The ability of hepatocytes to be infected with dengue virus serotype 2 in vitro support evidence implicating human hepatocytes as a target cell in cases of dengue virus infection, and provide the first experimental evidence to support the large number of clinical studies that implicate the liver as a critical target organ in severe cases of dengue infection.

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Kinetic analysis of cytokine response to cigarette smoke condensate by human endothelial and monocytic cells

Cited by 38 publications

References 27 publications

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

Phagocytosis and Inflammation: Exploring the effects of the components of E-cigarette vapor on macrophages

Regulated complement deposition on the surface of human endothelial cells: Effect of tobacco smoke and shear stress

Infection of human primary hepatocytes with dengue virus serotype 2

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