Uranium induces TNFα secretion and MAPK activation in a rat alveolar macrophage cell line

Gazin, Vincent; Kerdine, Saadia; Grillon, G.; Pallardy, Marc; Raoul, Hervé

doi:10.1016/j.taap.2003.08.016

Cited by 57 publications

(28 citation statements)

References 64 publications

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“…The binding of the TLR4/MD-2 complex receptor by microbial products triggers a downstream signaling cascade, culminating in the activation of nuclear transcription factor-kappa B (NF)-B, which promoter recognition sites directs the production of a number of pro-inflammatory cytokines, such as TNF-␣, IL-1␤ and IL-6 [29,30]. Myeloid differentiation protein 88 (MyD88) is involved in the main intracellular recruitment of adapter proteins [31,32]. Based on these roles, we suppose that the underling mechanism of attenuating the response of AMs to LPS by MD-2 silencing may be related to the TLR4/MyD88 signal pathway.…”

Section: Groupmentioning

confidence: 99%

Myeloid differentiation protein 2 silencing decreases LPS-induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages

Ren

Feng

et al. 2011

Immunology Letters

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Section: Groupmentioning

confidence: 99%

Myeloid differentiation protein 2 silencing decreases LPS-induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages

Ren

Feng

et al. 2011

Immunology Letters

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“…The mannose receptor is an important phagocytic and endocytic receptor critical for immune response and host defense. The attributes of this cell line have been exploited in numerous studies of the health impacts of environmental particles (Riley et al 2005;Gazin et al 2004;Fach et al 2002;Lane et al 1998;Long et al 1997). Per ATCC protocol, cultures are maintained by transferring floating cells to additional flasks-the floating cells are functionally normal.…”

Section: Rat Alveolar Macrophagesmentioning

confidence: 99%

A Macrophage-Based Method for the Assessment of the Reactive Oxygen Species (ROS) Activity of Atmospheric Particulate Matter (PM) and Application to Routine (Daily-24 h) Aerosol Monitoring Studies

Landreman

Shafer

Hemming

et al. 2008

Aerosol Science and Technology

147

133

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Both short-and long-term exposure to particulate matter (PM) air pollution have been demonstrated to cause increases in cardiovascular disease, cancer, and respiratory disorders. Although the specific mechanisms by which exposure to PM cause these affects are unclear, significant evidence has accumulated to suggest that PM exposure leads to increased inflammation as the result of excessive production of reactive oxygen species (ROS) in critical cell types. In order to better understand how real-world PM exposure causes adverse health effects, there is a need to efficiently integrate metrics of PM toxicity into large scale air monitoring and health effects/epidemiology studies. Here we describe a rapid, inexpensive, method that can be employed to assess the potential of sub-mg masses of PM to generate oxidative stress in alveolar macrophage cells. Importantly, the approach is compatible with routine daily PM sampling programs such as those administered by EPA (Speciation trends network (STN), IMPROVE network, PM2.5 mass monitoring network), allowing for multiple samples to be assessed simultaneously with low volumes and brief exposure periods. We apply the method to a set of water extracts of daily PM2.5 samples (25-350 µg PM mass) collected in the Denver-Metro area. Variations in the magnitude of the ROS response observed between the samples were only partially explained by differences in mass loading, with the highest levels of ROS being observed in samples collected during the summer months. This assay provides a very useful tool that can be coupled with detailed chemical analysis and statistical models to work towards the goal of attributing PM toxicity to specific real-world chemical sources.

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“…Uranium toxic studies in lung reported the toxic response to the metal. In macrophage cell line increased secretion of TNFα in association with JNK and P38 activation has been reported (Gazin et al 2004). The impact of cancer risk upon uranium exposure is worked out in epidemiological studies.…”

Section: Introductionmentioning

confidence: 97%

Uranium induces oxidative stress in lung epithelial cells

et al. 2006

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Uranium compounds are widely used in the nuclear fuel cycle, antitank weapons, tank armor, and also as a pigment to color ceramics and glass. Effective management of waste uranium compounds is necessary to prevent exposure to avoid adverse health effects on the population. Health risks associated with uranium exposure includes kidney disease and respiratory disorders. In addition, several published results have shown uranium or depleted uranium causes DNA damage, mutagenicity, cancer and neurological defects. In the current study, uranium toxicity was evaluated in rat lung epithelial cells. The study shows uranium induces significant oxidative stress in rat lung epithelial cells followed by concomitant decrease in the antioxidant potential of the cells. Treatment with uranium to rat lung epithelial cells also decreased cell proliferation after 72 h in culture. The decrease in cell proliferation was attributed to loss of total glutathione and superoxide dismutase in the presence of uranium. Thus the results indicate the ineffectiveness of antioxidant system's response to the oxidative stress induced by uranium in the cells.

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Uranium induces TNFα secretion and MAPK activation in a rat alveolar macrophage cell line

Cited by 57 publications

References 64 publications

Myeloid differentiation protein 2 silencing decreases LPS-induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages

Myeloid differentiation protein 2 silencing decreases LPS-induced cytokine production and TLR4/MyD88 pathway activity in alveolar macrophages

A Macrophage-Based Method for the Assessment of the Reactive Oxygen Species (ROS) Activity of Atmospheric Particulate Matter (PM) and Application to Routine (Daily-24 h) Aerosol Monitoring Studies

Uranium induces oxidative stress in lung epithelial cells

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