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Exposure of activated alveolar macrophages to brominated flame retardants augments the release of pro‐inflammatory cytokines in vitro
Author(s) -
Hennigar Stephen R,
Ronan Anne M,
Myers Jay L,
Tagliaferro Anthony R
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.724.6
Subject(s) - polybrominated diphenyl ethers , chemistry , inflammation , tumor necrosis factor alpha , immune system , incubation , alveolar macrophage , cytokine , inhalation , in vitro , proinflammatory cytokine , pharmacology , andrology , pollutant , immunology , environmental chemistry , macrophage , biochemistry , biology , medicine , anatomy , organic chemistry
Several environmental pollutants have been shown to have adverse effects on immune function that may result in respiratory conditions. In addition to diet, inhalation of dust is a major route of exposure of polybrominated diphenyl ethers (PBDEs) however; the impact of PBDEs on the immune response is unclear. The objective of this in vitro study was to determine the impact of physiological levels of PBDEs on the release of the pro‐inflammatory cytokine, TNFα, by activated alveolar macrophages. Porcine alveolar macrophages were seeded in three 24‐well plates in RPMI growth media supplemented with 10% porcine serum and incubated for 24‐hours (5% CO 2 , 37°C). After 24‐hours, the cells were activated by inoculation with PMA (0.01 mg/ml) and ionomycin (0.05 mg/ml) in 1% DMSO. In addition to the activating stimulus, three different concentrations of the PBDE mixture DE‐71 in MeOH were introduced to the wells (500 ng/mL DE‐71, 0.02% MeOH; 1000 ng/mL DE‐71, 0.04% MeOH; 2000 ng/mL DE‐71, 0.08% MeOH) (n = 9 per treatment). After 6‐hour incubation, conditioned media was removed, centrifuged, and stored at −80°C until analysis of TNFα via ELISA. Compared to controls, cells exposed to PMA and 1000 and 2000 ng/mL of PBDEs released 33 and 28% more TNFα, respectively (p < 0.05). As increased TNFα may indicate an increase in inflammation, findings suggest that chronic exposure to airborne PBDEs may be a cause of chronic respiratory inflammation. UNH Experimental Station Project H495. Grant Funding Source : UNH Experimental Station Project H495