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Int. J. Environ. Res. Public Health 2005, 2(1), 107-113; doi:10.3390/ijerph2005010107

Diesel Exhaust Particles Induce the Over expression of Tumor Necrosis Factor-α (TNF-α) Gene in Alveolar Macrophages and Failed to Induce Apoptosis through Activation of Nuclear Factor-κB (NF-κB)

Center of Environmental Health and Molecular Toxicology Laboratory, Jackson State University, Jackson, Mississippi, USA
Human Exposure Section, United States Environmental Protection Agency, Chapel Hill, North Carolina
Author to whom correspondence should be addressed.
Received: 15 November 2004 / Accepted: 6 February 2005 / Published: 30 April 2005
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Exposure to particulate matter (PM2.5-10), including diesel exhaust particles (DEP) has been reported to induce lung injury and exacerbation of asthma and chronic obstructive pulmonary disease. Alveolar macrophages play a major role in the lung’s response to inhaled particles and therefore, are a primary target for PM2.5-10 effect. The molecular and cellular events underlying DEP-induced toxicity in the lung, however, remain unclear. To determine the effect of DEP on alveolar macrophages, RAW 264.7 cells were grown in RPMI 1640 with supplements until confluency. RAW 264.7 cultures were exposed to Hank’s buffered saline solution (vehicle), vehicle containing an NF-κB inhibitor, BAY11-7082 (25μM with 11/2 hr pre-incubation), or vehicle containing DEP (250μg/ml) in the presence or absence of BAY11-7082 (25μM with 11/2 hr pre-incubation) for 4 hr and TNF-α release was determined by enzyme-linked immunosorbent assay and confirmed by western blots. RAW 264.7 apoptotic response was determined by DNA fragmentation assays. U937 cells treated with campothecin (4 μg/ml x 3 hr), an apoptosis-inducing agent, were used as positive control. We report that exposure to the carbonaceous core of DEP induces significant release of TNF-α in a concentration-dependent fashion (31 ± 4 pg/ml, n = 4, p = 0.08; 162 ± 23 pg/ml, n = 4, p < 0.05; 313 ± 31 pg/ml, n = 4, p < 0.05 at 25, 100, and 250 μg/ml, respectively). DEP exposure, however, failed to induce any apoptotic response in RAW 264.7 cells. Moreover, inhibition of NF-κB binding activity has resulted in DEP-induced apoptotic response in alveolar macrophages, as demonstrated by the NF-κB inhibitor, BAY11-7082 studies. The results of the present study indicate that DEP induce the release of TNF-α in alveolar macrophages, a primary target for inhaled particles effect. DEP-induced TNF-α gene expression is regulated at the transcriptional level by NF-κB. Furthermore, DEP-induced increase in NF-κB-DNA binding activity appears to protect against apoptosis. View Full-Text

This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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MDPI and ACS Style

Kafoury, R.M.; Madden, M.C. Diesel Exhaust Particles Induce the Over expression of Tumor Necrosis Factor-α (TNF-α) Gene in Alveolar Macrophages and Failed to Induce Apoptosis through Activation of Nuclear Factor-κB (NF-κB). Int. J. Environ. Res. Public Health 2005, 2, 107-113.

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