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Significance of persistent inflammation in respiratory disorders induced by nanoparticles.

Morimoto Y, Izumi H, Kuroda E - J Immunol Res (2014)

Bottom Line: Chemical and physical damage are associated with point mutation by free radicals and double strand brake, respectively.Nanoparticles and asbestos also induce the production of free radicals.In allergic responses, nanoparticles act as Th2 adjuvants to activate Th2 immune responses such as activation of eosinophil and induction of IgE.

View Article: PubMed Central - PubMed

Affiliation: Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan.

ABSTRACT
Pulmonary inflammation, especially persistent inflammation, has been found to play a key role in respiratory disorders induced by nanoparticles in animal models. In inhalation studies and instillation studies of nanomaterials, persistent inflammation is composed of neutrophils and alveolar macrophages, and its pathogenesis is related to chemokines such as the cytokine-induced neutrophil chemoattractant (CINC) family and macrophage inflammatory protein-1α and oxidant stress-related genes such as heme oxygenase-1 (HO-1). DNA damages occur chemically or physically by nanomaterials. Chemical and physical damage are associated with point mutation by free radicals and double strand brake, respectively. The failure of DNA repair and accumulation of mutations might occur when inflammation is prolonged, and finally normal cells could become malignant. These free radicals can not only damage cells but also induce signaling molecules containing immunoreaction. Nanoparticles and asbestos also induce the production of free radicals. In allergic responses, nanoparticles act as Th2 adjuvants to activate Th2 immune responses such as activation of eosinophil and induction of IgE. Taken together, the presence of persistent inflammation may contribute to the pathogenesis of a variety of diseases induced by nanomaterials.

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Related in: MedlinePlus

Tentative relationship between inflammation by nanomaterials and malignant tumor.
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Related In: Results  -  Collection


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fig2: Tentative relationship between inflammation by nanomaterials and malignant tumor.

Mentions: We performed intratracheal instillations of different mineral fibers to rats and examined lung inflammation from 3 days up to 6 months [17]. Harmful respirable particles like crystalline silica or crocidolite asbestos, which are kinds of asbestos, caused persistent inflammation from the initial instillation until 6 months later. However, when less harmful micron-sized titanium dioxide was inhaled, transient inflammation was only observed early in the instillation. As for crystalline silica, an exacerbation of inflammation was found in the lung after 1 or 2 months after exposure. Sellamuthu et al. [18] reported that when rats were exposed to inhalation of crystalline silica (15 mg/m3, 6 h/day, 5 days), pulmonary damage was determined after the latent periods (0–16 weeks). The number of neutrophils and the concentration of MCP-1 in BALF were maximum after 16 weeks. Langley et al. [19] conducted a 6-week inhalation of silica with 27 weeks after exposure, and the number of neutrophils and lymphocytes in BALF increased 10 weeks after exposure, although not at 4 days, and LDH and protein concentration in BALF significantly increased at 10 and 17 weeks, but not at 4 days. Kobayashi et al. [16] showed that different evaluations of pulmonary toxicity by intratracheal instillation of titanium dioxide nanoparticles can be derived on the basis of observations up to 1 week after instillation and those after 1 month after instillation. Based on the results of intratracheal instillation studies and inhalation studies, both short-and long-term effects (from 3 days up to 6 months) should be evaluated when assessing the toxicity, including persistent inflammation, of nanoparticles. Therefore we speculate that exposure of the high toxic nanomaterial may induce persistent inflammation in the lung through the persistent production of chemokines, such as CINC, MIP, and MCP, and that sustained production of proteinases and ROS cause the lung injury during these chronic inflammations. Fujita et al. [7] reported that exposure to nickel oxide nanoparticle following intratracheal instillation induced persistent proteinases such as MMP-12 in rat lung.


Significance of persistent inflammation in respiratory disorders induced by nanoparticles.

Morimoto Y, Izumi H, Kuroda E - J Immunol Res (2014)

Tentative relationship between inflammation by nanomaterials and malignant tumor.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4109676&req=5

fig2: Tentative relationship between inflammation by nanomaterials and malignant tumor.
Mentions: We performed intratracheal instillations of different mineral fibers to rats and examined lung inflammation from 3 days up to 6 months [17]. Harmful respirable particles like crystalline silica or crocidolite asbestos, which are kinds of asbestos, caused persistent inflammation from the initial instillation until 6 months later. However, when less harmful micron-sized titanium dioxide was inhaled, transient inflammation was only observed early in the instillation. As for crystalline silica, an exacerbation of inflammation was found in the lung after 1 or 2 months after exposure. Sellamuthu et al. [18] reported that when rats were exposed to inhalation of crystalline silica (15 mg/m3, 6 h/day, 5 days), pulmonary damage was determined after the latent periods (0–16 weeks). The number of neutrophils and the concentration of MCP-1 in BALF were maximum after 16 weeks. Langley et al. [19] conducted a 6-week inhalation of silica with 27 weeks after exposure, and the number of neutrophils and lymphocytes in BALF increased 10 weeks after exposure, although not at 4 days, and LDH and protein concentration in BALF significantly increased at 10 and 17 weeks, but not at 4 days. Kobayashi et al. [16] showed that different evaluations of pulmonary toxicity by intratracheal instillation of titanium dioxide nanoparticles can be derived on the basis of observations up to 1 week after instillation and those after 1 month after instillation. Based on the results of intratracheal instillation studies and inhalation studies, both short-and long-term effects (from 3 days up to 6 months) should be evaluated when assessing the toxicity, including persistent inflammation, of nanoparticles. Therefore we speculate that exposure of the high toxic nanomaterial may induce persistent inflammation in the lung through the persistent production of chemokines, such as CINC, MIP, and MCP, and that sustained production of proteinases and ROS cause the lung injury during these chronic inflammations. Fujita et al. [7] reported that exposure to nickel oxide nanoparticle following intratracheal instillation induced persistent proteinases such as MMP-12 in rat lung.

Bottom Line: Chemical and physical damage are associated with point mutation by free radicals and double strand brake, respectively.Nanoparticles and asbestos also induce the production of free radicals.In allergic responses, nanoparticles act as Th2 adjuvants to activate Th2 immune responses such as activation of eosinophil and induction of IgE.

View Article: PubMed Central - PubMed

Affiliation: Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Japan.

ABSTRACT
Pulmonary inflammation, especially persistent inflammation, has been found to play a key role in respiratory disorders induced by nanoparticles in animal models. In inhalation studies and instillation studies of nanomaterials, persistent inflammation is composed of neutrophils and alveolar macrophages, and its pathogenesis is related to chemokines such as the cytokine-induced neutrophil chemoattractant (CINC) family and macrophage inflammatory protein-1α and oxidant stress-related genes such as heme oxygenase-1 (HO-1). DNA damages occur chemically or physically by nanomaterials. Chemical and physical damage are associated with point mutation by free radicals and double strand brake, respectively. The failure of DNA repair and accumulation of mutations might occur when inflammation is prolonged, and finally normal cells could become malignant. These free radicals can not only damage cells but also induce signaling molecules containing immunoreaction. Nanoparticles and asbestos also induce the production of free radicals. In allergic responses, nanoparticles act as Th2 adjuvants to activate Th2 immune responses such as activation of eosinophil and induction of IgE. Taken together, the presence of persistent inflammation may contribute to the pathogenesis of a variety of diseases induced by nanomaterials.

Show MeSH
Related in: MedlinePlus