Nano Titanium Dioxide Particles Promote Allergic Sensitization and Lung Inflammation in Mice

Larsen, SÃ ̧ren T.; Roursgaard, Martin; Jensen, Keld Alstrup; Nielsen, Gunnar D.

doi:10.1111/j.1742-7843.2009.00473.x

Cited by 118 publications

(91 citation statements)

References 31 publications

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“…For example, carbon black ultrafine particles, titanium dioxide nanoparticles, carbon nanotubes, and diesel exhaust particles have all been shown to promote allergic sensitization and AAI (5,6,(8)(9)(10)(11)(12)(13)(14). However, there are some important differences between these studies and ours.…”

Section: Discussioncontrasting

confidence: 49%

“…Indeed, ambient pollutant particles and diesel exhaust particles can promote lung inflammation and allergic sensitization (5)(6)(7)(8). Studies have also shown that carbon black nanoparticles (9)(10)(11), titanium dioxide nanoparticles (12), and carbon nanotubes (13,14) can promote allergic sensitization, allergic airway inflammation (AAI), and/or stimulate dendritic cell (DC) and allergen-specific T cells. However, a significant component of these particle adjuvant effects has been attributed to adsorbed toxic chemicals and metallic impurities and the ability to induce oxidative stress (6,7,13,(15)(16)(17)(18)(19).…”

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confidence: 99%

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Inert 50-nm Polystyrene Nanoparticles That Modify Pulmonary Dendritic Cell Function and Inhibit Allergic Airway Inflammation

Hardy

Lemasurier

Belz

et al. 2012

The Journal of Immunology

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Nanoparticles are being developed for diverse biomedical applications, but there is concern about their potential to promote inflammation, particularly in the lung. Although a variety of ambient, anthropogenic and man-made nanoparticles can promote lung inflammation, little is known about the long-term immunomodulatory effects of inert noninflammatory nanoparticles. We previously showed polystyrene 50-nm nanoparticles coated with the neutral amino acid glycine (PS50G nanoparticles) are not inflammatory and are taken up preferentially by dendritic cells (DCs) in the periphery. We tested the effects of such nanoparticles on pulmonary DC function and the development of acute allergic airway inflammation. Surprisingly, exposure to PS50G nanoparticles did not exacerbate but instead inhibited key features of allergic airway inflammation including lung airway and parenchymal inflammation, airway epithelial mucus production, and serum allergen-specific IgE and allergen-specific Th2 cytokines in the lung-draining lymph node (LN) after allergen challenge 1 mo later. PS50G nanoparticles themselves did not induce lung oxidative stress or cardiac or lung inflammation. Mechanistically, PS50G nanoparticles did not impair peripheral allergen sensitization but exerted their effect at the lung allergen challenge phase by inhibiting expansion of CD11c+MHCIIhi DCs in the lung and draining LN and allergen-laden CD11bhiMHCIIhi DCs in the lung after allergen challenge. PS50G nanoparticles further suppressed the ability of CD11bhi DCs in the draining LN of allergen-challenged mice to induce proliferation of OVA-specific CD4+ T cells. The discovery that a defined type of nanoparticle can inhibit, rather than promote, lung inflammation via modulation of DC function opens the door to the discovery of other nanoparticle types with exciting beneficial properties.

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Section: Discussioncontrasting

confidence: 49%

mentioning

confidence: 99%

Inert 50-nm Polystyrene Nanoparticles That Modify Pulmonary Dendritic Cell Function and Inhibit Allergic Airway Inflammation

Hardy

Lemasurier

Belz

et al. 2012

The Journal of Immunology

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show abstract

“…Evidence suggests that ambient ultrafine particles (,100 nm) play a disproportionate role in asthma exacerbations compared with fine-sized microparticles (100-2500 nm) (2-5), suggesting that inhaled particle size influences their relative ability to modulate lung function. Similarly, man-made carbon black and titanium dioxide nanoparticles (6)(7)(8) and carbon nanotubes (9,10) all promote allergic sensitization and/or allergic airway inflammation (AAI). However, counterintuitively, we recently made the discovery that preadministration of inert nontoxic polystyrene nanoparticles 50 nm in diameter (PS50G), which do not induce oxidative stress, can inhibit development of AAI by impairing pulmonary dendritic cell (DC) expansion or stimulatory function (11).…”

mentioning

confidence: 99%

Differential Uptake of Nanoparticles and Microparticles by Pulmonary APC Subsets Induces Discrete Immunological Imprints

Hardy

Lemasurier

Mohamud

et al. 2013

The Journal of Immunology

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There is increasing interest in the use of engineered particles for biomedical applications, although questions exist about their proinflammatory properties and potential adverse health effects. Lung macrophages and dendritic cells (DC) are key regulators of pulmonary immunity, but little is known about their uptake of different sized particles or the nature of the induced immunological imprint. We investigated comparatively the immunological imprints of inert nontoxic polystyrene nanoparticles 50 nm in diameter (PS50G) and 500 nm in diameter (PS500G). Following intratracheal instillation into naive mice, PS50G were preferentially taken up by alveolar and nonalveolar macrophages, B cells, and CD11b+ and CD103+ DC in the lung, but exclusively by DC in the draining lymph node (LN). Negligible particle uptake occurred in the draining LN 2 h postinstillation, indicating that particle translocation does not occur via lymphatic drainage. PS50G but not PS500G significantly increased airway levels of mediators that drive DC migration/maturation and DC costimulatory molecule expression. Both particles decreased frequencies of stimulatory CD11b+MHC class IIhi allergen-laden DC in the draining LN, with PS50G having the more pronounced effect. These distinctive particle imprints differentially modulated induction of acute allergic airway inflammation, with PS50G but not PS500G significantly inhibiting adaptive allergen-specific immunity. Our data show that nanoparticles are taken up preferentially by lung APC stimulate cytokine/chemokine production and pulmonary DC maturation and translocate to the lung-draining LN via cell-associated transport. Collectively, these distinctive particle imprints differentially modulate development of subsequent lung immune responses. These findings support the development of lung-specific particulate vaccines, drug delivery systems, and immunomodulators.

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“…Immunomodulation have been also observed in in vivo studies (Skocaj et al 2011). Larsen et al (2010) found increased levels of immunoglobulins IgE and IgG1 in the serum and appearance of of eosinophils, neutrophils and lymphocytes in bronchoalveolar lavage fluid after intraperitoneal TiO 2 NPs intake. In the present study, oral administration of carnosine or melatonin showed significant reduced levels of all the studied parameters as they were antioxidants, thus opposed the cytotoxic effects of TiO 2-NPs due to their physicochemical properties can lead to the generation of reactive oxygen species, resulting their accumulation, which in turn, reduce the activities of antioxidant enzymes and antioxidant contents (Warheit et al 2007;Sheng et al 2013).…”

Section: Discussionmentioning

confidence: 83%

“…These studies were in agreement with the present study, which revealed that as regard cardiac functions parameters represented by myoglobin, troponinT and creatine kinase MB isozyme, the results of this study showed significant increase in these parameters, both at low and high doses of TiO2-NPs treated rats. Larsen et al (2010) found that intraperitoneal TiO 2 NPs in mice, lead to liver, kidney and cardiovascular damage indicated by the elevated serum markers of these organs. These elevation were higher in mice treated with NP TiO 2 than those treated with submicron-sized TiO 2 .…”

Section: Discussionmentioning

confidence: 99%

Role of Carnosine and Melatonin in Ameliorating Cardiotoxicity of Titanium Dioxide Nanoparticles in the Rats

Al-Rasheed¹,

Faddah²,

Ibrahim

et al. 2015

Braz. arch. biol. technol.

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The aim of this work was to study the possible cardiotoxicity of two different doses of 50 nm nano titanium dioxide (n-TiO 2 ) and the possible modulating effects of the use of two natural antioxidants carnosine and melatonin. The results showed that TiO 2-NPs produced deleterious effects on rat cardiac tissue as confirmed by the increased levels of serum myoglobin, troponin-T and CK-MB. Increased levels of serum Inflammatory markers represented by the tumor necrosis factor alpha (TNF-α) and

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Nano Titanium Dioxide Particles Promote Allergic Sensitization and Lung Inflammation in Mice

Cited by 118 publications

References 31 publications

Inert 50-nm Polystyrene Nanoparticles That Modify Pulmonary Dendritic Cell Function and Inhibit Allergic Airway Inflammation

Inert 50-nm Polystyrene Nanoparticles That Modify Pulmonary Dendritic Cell Function and Inhibit Allergic Airway Inflammation

Differential Uptake of Nanoparticles and Microparticles by Pulmonary APC Subsets Induces Discrete Immunological Imprints

Role of Carnosine and Melatonin in Ameliorating Cardiotoxicity of Titanium Dioxide Nanoparticles in the Rats

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