Diesel exhaust particles induced release of interleukin 6 and 8 by (primed) human bronchial epithelial cells (BEAS 2b) in vitro

Steerenberg, P. A.; Zonnenberg, J.A.J.; Dormans, J. A. M. A.; Joon, P.N.T.; Wouters, I.M.; Bree, L. van; Scheepers, Paul T.J.; Loveren, Henk Van

doi:10.1016/s0165-2478(97)85744-6

Cited by 18 publications

(26 citation statements)

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“…The literature reports on the response of cultured cells to specific particle types, such as silica, shows complex and somewhat inconsistent patterns. Our observed response to Min-U-Sil and TiO 2 can be compared to the results of Steerenberg et al, [49] who reported no increase over control for IL-6 in BEAS-2B cells treated with TiO 2 , comparable responses for diesel particles and α-quartz (17 ± 16 and 11 ± 15 fold), and higher response (59 ± 57 fold) response to fumed silica. Steerenberg's results suggest that different silica preparations have different potency, and that the IL-6 response of BEAS-2B cells is highly variable as indicated in Steerenberg's data where the standard deviation of IL-6 was comparable to the mean.…”

Section: Discussionsupporting

confidence: 85%

“…In another study, DQ12 quartz was more cytotoxic than silicasol particles (60 and 100 nm) and neither quartz or silicasol nanoparticles induced IL-6 in A549 cells. [45] Micron-sized TiO 2 is sometimes considered an inert particle and used as a negative control in particle studies, [30,49] but other studies have shown that nano-TiO 2 can be proinflammatory in vivo [47,51] and can be taken up by nonphagocytic mechanisms by macrophages in vitro [52]. …”

Section: Discussionmentioning

confidence: 99%

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Cytokine responses of human lung cells (BEAS-2B) treated with micron-sized and nanoparticles of metal oxides compared to soil dusts

et al. 2007

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Background: The induction of cytokines by airway cells in vitro has been widely used to assess the effects of ambient and occupational particles. This study measured cytotoxicity and the release of the proinflammatory cytokines IL-6 and IL-8 by human bronchial epithelial cells treated with manufactured nano-and micron-sized particles of Al 2 O 3 , CeO 2 , Fe 2 O 3 , NiO, SiO 2 , and TiO 2 , with soil-derived particles from fugitive dust sources, and with the positive controls LPS, TNF-α, and VOSO 4 .

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Cytokine responses of human lung cells (BEAS-2B) treated with micron-sized and nanoparticles of metal oxides compared to soil dusts

et al. 2007

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“…Previous studies have reported DE-induced increases in IL-6 and IL-8 in cultured bronchial epithelial cells (Steerenberg et al, 1998). Similarly, we noted significant increases in IL-6 and IL-8 mRNA expression in lungs of younger and older animals after exposure to DE (single or repeated).…”

Section: Discussionmentioning

confidence: 92%

Pulmonary effects of inhaled diesel exhaust in aged mice

Sunil

Patel

Mainelis

et al. 2009

Toxicology and Applied Pharmacology

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Pulmonary morbidity and mortality resulting from exposure to fine particulate matter (PM) increases with age. The present studies analyzed potential mechanisms underlying increased susceptibility of the elderly to PM using diesel exhaust (DE) as a model. Mice (2 m and 18 m) were exposed to DE (0, 300, and 1000 μg/m 3 ) for 3 h once (single) or 3 h/day for 3 days (repeated). Bronchoalveolar lavage fluid (BAL), serum and lung tissue were collected 0 and 24 h later. Exposure to DE resulted in structural alterations in the lungs of older but not younger mice, including patchy thickening of the alveolar septa and inflammatory cell localization in alveolar spaces. These effects were most pronounced 24 h after a single exposure to the higher dose of DE. Significant increases in BAL nitrogen oxides were also noted in older mice, as well as expression of lipocalin 24p3, an oxidative stress marker in the lung with no effects in younger mice. Following DE inhalation, expression of Tumor Necrosis Factor alpha (TNFα) was upregulated in lungs of both younger and older mice; however, this was attenuated in older animals. Whereas exposure to DE resulted in increases in lung Interleukin-6 (IL-6) expression in both older and younger mice, IL-8 increased only in older animals. In younger mice, constitutive expression of manganese superoxide dismutase (MnSOD) decreased after DE exposure, while in older mice, constitutive MnSOD was not detectable and DE had no effect on expression of this antioxidant. Taken together, these results suggest that altered generation of inflammatory mediators and MnSOD may contribute to increased susceptibility of older mice to inhaled DE.

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“…In relation to this, macrophages, monocytes and dendritic cells (DCs) of different origins exposed to a-quartz in vitro have been demonstrated to enhance mRNA expression or protein production of IL-8 [a potent chemokine for PMN (Allen & Kurdowska, 2014)] (Xu et al, 2003) and MIP-2 (Rao et al, 2004;Sayes et al, 2007), although Zeidler et al (2003) failed to demonstrate enhanced MIP-2 production in murine bronchoalveolar lavage cells exposed to a-quartz. Alveolar epithelial cells of different origins also produce protein or enhanced expression of mRNA for IL-8 (Monteiller et al, 2007;Øvrevik et al, 2004;Seagrave & Nikula, 2000;Schins et al, 2000;Singh et al, 2007;Steerenberg et al, 1998;Stringer et al, 1996;Xu et al, 2003;Wottrich et al, 2004) and MIP-2 (Driscoll et al, 1996;Øvrevik et al, 2004) in response to a-quartz. Collectively, it is highly likely that inhaled a-quartz directly stimulates epithelial cells to produce PMN chemokines in the lung, but the direct contribution of a-quartz to MIP-2 production in macrophages needs further research.…”

Section: Inflammatory Reactions and Fibrosis In The Lungmentioning

confidence: 99%

A mechanistic review of silica-induced inhalation toxicity

Kawasaki

2015

Inhalation Toxicology

112

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Crystalline forms of silica have been proposed as positive control material for the toxicity test of inhaled particulate/fibrous matter, although mechanism of silica-induced inhalation toxicity has not yet been established. Inhalation exposure of α-quartz to rodents induces severe lung inflammation and fibrosis only after a certain period of latency, despite strong surface reactivity. The delayed occurrence of inhalation toxicity by α-quartz may be largely attributed to the sequestration of α-quartz particles by alternatively activated (M2) macrophages that express abundant levels of scavenger receptors but are relatively insensitive to inflammatory stimuli. When exposure to α-quartz continues, lung dust burden reaches a particle overload level, at which M2 macrophages cannot accommodate further quartz particles. Free quartz particles distributed in the interstitium interact with another subtype of macrophages, classically activated/inflammatory (M1) macrophages, which secrete various inflammatory cytokines, but silica-laden M1 macrophages initiate granuloma formation, which sequesters silica particles, too. Furthermore, the ability of M2 macrophages to clear foreign matter, particularly bacterial endotoxins [lipopolysaccharides (LPS)], may decrease due to α-quartz cytotoxicity. When LPS concentration in the lung reaches a certain level, LPS primes M1 macrophages to prepare for interleukin-1β production in response to α-quartz and also stimulates M1 macrophages and plasmacytoid dendritic cells (pDCs) to produce tumor necrosis factor (TNF)-α and interferon (IFN)-β, respectively. Besides, IFN-β may enhance TNF-α production in LPS-stimulated M1 macrophages. The elevated levels of inflammatory cytokines produce progressive lung inflammation and fibrosis.

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Diesel exhaust particles induced release of interleukin 6 and 8 by (primed) human bronchial epithelial cells (BEAS 2b) in vitro

Cited by 18 publications

References 0 publications

Cytokine responses of human lung cells (BEAS-2B) treated with micron-sized and nanoparticles of metal oxides compared to soil dusts

Cytokine responses of human lung cells (BEAS-2B) treated with micron-sized and nanoparticles of metal oxides compared to soil dusts

Pulmonary effects of inhaled diesel exhaust in aged mice

A mechanistic review of silica-induced inhalation toxicity

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