In vitro toxicity evaluation of diesel exhaust particles on human eosinophilic cell

Hirota, Ryoji; Akimaru, Kunihiro; Nakamura, Hiroyuki

doi:10.1016/j.tiv.2008.02.004

Cited by 19 publications

(9 citation statements)

References 26 publications

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“…Consistent with this, we and others have previously demonstrated that DEP exposure induces and/or aggravates airway inflammation in atopic/allergic animals, including NC/Nga mice (which naturally develop an atopic dermatitis-like pathophysiology; Takano et al, 1997;Ichinose et al, 1998;Inoue et al, 2005a). Furthermore, DEP reportedly affect/disrupt several cell populations, which contributes to their immunotoxicity, such as epithelial cells (Terada et al, 1997;Takizawa et al, 2003), endothelial cells (Terada et al, 1999), macrophages (Beck-Speier et al, 2005), eosinophils (Hirota et al, 2008), dendritic cells (DC: Inoue et al, 2009), and mast cells/basophils (Saneyoshi et al, 1997;Devouassoux et al, 2002), mainly in vitro. Generally, peripheral lymphoid organs such as the spleen and their resident mononuclear cells including lymphocytes, are key players in the immunopathogenesis of allergy; thus, the effects of DEP on these compartments may provide much information on their adjuvant effects.…”

Section: Introductionsupporting

confidence: 86%

In vitro study of the effect of nanoparticle-rich diesel exhaust particles on IL-18 production in splenocytes

et al. 2011

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-It has been shown that pulmonary exposure to diesel exhaust particles (DEP) disrupts the immune system, presenting as exacerbating effects on allergic manifestations (e.g., allergic asthma). However, since a model inhalation system has not been developed, the impact of nano-level DEP on health has not been satisfactorily investigated. Our institute (the National Institute for Environmental Studies) established an "environmental nanoparticle exposure system applied in animals" in 2005 and since then, we have explored the health effects of exposure to these types of agent. The present study was conducted to investigate the in vitro effects of nanoparticle-rich DEP (NRDEP) on primary splenocytes from atopyprone hosts. NC/Nga mouse-derived splenic mononuclear cells were co-cultured with NRDEP (0-50 μg/ ml); thereafter, the production/release of interleukin (IL)-18 in the culture supernatants was evaluated by means of ELISA. NRDEP increased IL-18 production/release by splenocytes in a dose-dependent manner with an overall trend (with significance vs. 10 μg/ml of NRDEP). In contrast, 50 μg/ml of NRDEP inhibited production/release. These results suggest that NRDEP can activate naïve splenic mononuclear cells from atopy-prone animals in terms of IL-18 induction.

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Section: Introductionsupporting

confidence: 86%

In vitro study of the effect of nanoparticle-rich diesel exhaust particles on IL-18 production in splenocytes

et al. 2011

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“…IL-8 is an important activator and chemoattractant for polymorphonuclear leukocytes and has been implicated in a variety of inflammatory diseases, such as asthma [41]. IL-8 protein is secreted at low levels from cells that have not been stimulated, but its production is rapidly induced by a wide range of stimuli encompassing proinflammatory cytokines [42], bacterial or viral products [43,44] and cellular stressors [45,46]. …”

Section: Discussionmentioning

confidence: 99%

Alternaria Fungus Induces the Production of GM-CSF, Interleukin-6 and Interleukin-8 and Calcium Signaling in Human Airway Epithelium through Protease-Activated Receptor 2

Matsuwaki

Wada

White

et al. 2012

Int Arch Allergy Immunol

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Rationale: Recent studies suggest that host immune responses to environmental fungi may play an important role in the development of allergic diseases, such as human asthma. Epithelium is considered an active participant in allergic inflammation. We previously reported that aspartate protease from Alternaria induces the activation and degranulation of human eosinophils that are mediated through protease-activated receptor 2 (PAR-2). However, our current knowledge on the innate immune responses of epithelium to environmental fungi is very limited. We investigated the responses of epithelium to fungi and the mechanisms of these responses. Methods: Human airway epithelial cell line BEAS-2B and Calu-3 (both from American Type Culture Collection) were incubated with PAR-2 peptides and extracts of various fungi. The cellular responses, including GM-CSF, interleukin (IL)-6, IL-8, eotaxin, eotaxin-2 and RANTES production as well as increases in intracellular calcium concentration ([Ca²⁺]_i), were examined. To characterize the proteases involved in these responses, protease inhibitors such as pepstatin A and alkalo-thermophilic Bacillus inhibitor (ATBI), HIV protease inhibitors and 4-amidinophenylmethanesulfonyl fluoride hydrochloride were used. To investigate the role of PAR-2, PAR-2-agonistic and PAR-2-antagonistic peptides were used. Results: PAR-2-activating peptide, but not the control peptide, induced GM-CSF, IL-6 and IL-8 production; these cellular responses were accompanied by a quick and marked increase in [Ca²⁺]_i. Among 7 common environmental fungi, only Alternaria induced GM-CSF, IL-6 and IL-8 production and increased [Ca²⁺]_i response. Both cytokine production and increased [Ca²⁺]_i were significantly inhibited by PAR-2 antagonist peptide and by aspartate protease inhibitors (pepstatin A, ritonavir, nelfinavir and ATBI), but not by the PAR-2 control peptide or by other protease inhibitors. Conclusions: Aspartate proteases from Alternaria induce cytokine production and calcium response in airway epithelium that is mediated through PAR-2. This protease-mediated activation of airway epithelium may be implicated in the development and exacerbation of airway allergic disease.

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“…Some studies report that exposure to diesel exhaust particles, PM 2.5 , and silica induced activation of NF-B in vitro and in vivo (Cho et al, 2003;Hirota et al, 2008;Shukla et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Expression of cytokine-induced neutrophil chemoattractant in rat lungs by intratracheal instillation of nickel oxide nanoparticles

Nishi

Morimoto

Ogami

et al. 2009

Inhalation Toxicology

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Since nanoparticles easily agglomerate to form larger particles, it is important to maintain the size of their agglomerates at the nano-level to evaluate the harmful effect of the nanoparticles. We prevented agglomeration of nickel oxide nanoparticles by ultrasound diffusion and filtration, established an acute exposure model using animals, and examined inflammation and chemokine expression. The mass median diameter of nickel oxide nanoparticle agglomerates suspended in distilled water for intratracheal instillation was 26 nm (8.41 nm weighted average surface primary diameter). Male Wistar rats received intratracheal instillation of nickel oxide nanoparticles at 0.1 mg (0.33 mg/kg) or 0.2 mg (0.66 mg/kg), and were dissected 3 days, 1 week, 1 month, 3 months, and 6 months after the instillation. The control group received intratracheal instillation of distilled water. Three chemokines (cytokine-induced neutrophil chemoattractant-1 (CINC-1), CINC-2alphabeta, and CINC-3) in the lung tissue and bronchoalveolar lavage fluid (BALF) were determined by quantitative measurement of protein by ELISA. Both CINC-1 and CINC-2alphabeta concentration was elevated from day 3 to 3 months in lung tissue and from day 3 to 6 months in BALF. On the other hand, CINC-3 was elevated on day 3 in both lung tissue and BALF, and then decreased. The total cell and neutrophil counts in BALF were increased from day 3 to 3 months. In lung tissue, infiltration of mainly neutrophils and alveolar macrophages was observed from day 3 to 6 months in alveoli. These results suggest that CINC was involved in lung injury by nickel oxide nanoparticles.

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In vitro toxicity evaluation of diesel exhaust particles on human eosinophilic cell

Cited by 19 publications

References 26 publications

In vitro study of the effect of nanoparticle-rich diesel exhaust particles on IL-18 production in splenocytes

In vitro study of the effect of nanoparticle-rich diesel exhaust particles on IL-18 production in splenocytes

Alternaria Fungus Induces the Production of GM-CSF, Interleukin-6 and Interleukin-8 and Calcium Signaling in Human Airway Epithelium through Protease-Activated Receptor 2

Expression of cytokine-induced neutrophil chemoattractant in rat lungs by intratracheal instillation of nickel oxide nanoparticles

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