Preexposure to Amorphous Silica Particles Attenuates but also Enhances Allergic Reactions in Trimellitic Anhydride-Sensitized Brown Norway Rats

Arts, J.H.E.; Schijf, Marcel A.; Kuper, C. Frieke

doi:10.1080/08958370802105371

Cited by 9 publications

(6 citation statements)

References 46 publications

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“…Exposure to SAS for 6 days prior to TMA challenge diminished the effect of TMA on tidal volume, laryngeal ulceration, laryngeal inflammation, and the number of BAL (lung) eosinophils in most animals, but aggravated laryngeal squamous metaplasia and inflammation in a single animal (Arts et al, 2008). The results of the present study are also in accordance with a few other experimental studies, using HMW allergens such as ovalbumin.…”

Section: Total Cells Eosinophils Neutrophils Lymphocytessupporting

confidence: 94%

Pre-exposure to sulfur dioxide attenuates most allergic reactions upon trimellitic anhydride challenge in sensitized Brown Norway rats

Arts

Jacobs

Kuper

2010

Inhalation Toxicology

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Irritant-induced inflammation of the airways may aggravate respiratory allergy induced by chemical respiratory allergens. Therefore, it was studied whether airway irritation by sulfur dioxide (SO(2)) would enhance respiratory allergic reactions to trimellitic anhydride (TMA), using a rat model. Brown Norway (BN) rats were topically sensitized, subsequently exposed for a single time or repeatedly to 300 ppm SO(2), and challenged by inhalation to a distinctly irritating or minimally irritating concentration of TMA after the (last) SO(2) exposure. Repeated exposure to SO(2) alone reduced breathing frequency during exposure, and caused epithelial alterations including hyperplasia and squamous metaplasia, and infiltration of polymorphonuclear inflammatory cells into nasal tissues, larynx, trachea, and bronchi/bronchioli. Histopathological changes were less prominent after 1 day of SO(2) exposure. Repeated pre-exposure to SO(2) reduced the number of TMA-induced apnoeas, in an SO(2) exposure duration-dependent manner. This effect of SO(2) on TMA-induced functional allergic reactions (apnoeas) was distinct only when the TMA challenge concentration was not too irritating itself. Repeated pre-exposure to SO(2) reduced TMA-induced laryngeal ulceration, goblet-cell hyperplasia, and inflammation in the lungs in most animals, regardless of the TMA challenge concentration. The SO(2)-induced replacement of normal respiratory epithelium by less sensitive, squamous epithelium may offer an explanation for the, unexpected, reduced allergic manifestation. However in a few animals, SO(2) appeared to facilitate TMA-induced irritation, probably due to incomplete protection. Overall, SO(2) exposure of TMA-sensitized rats reduced TMA-related allergic respiratory responses in most animals.

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Section: Total Cells Eosinophils Neutrophils Lymphocytessupporting

confidence: 94%

Pre-exposure to sulfur dioxide attenuates most allergic reactions upon trimellitic anhydride challenge in sensitized Brown Norway rats

Arts

Jacobs

Kuper

2010

Inhalation Toxicology

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“…Arts et al [153] examined the effect of pre-exposure to synthetic (fumed) amorphous SNPs (14 nm) on elicitation of airway hypersensitivity reactions by the low-molecular-weight allergen trimellitic anhydride (TMA). Brown Norway rats were topically sensitized with TMA, exposed (head or nose only) to SNPs for 6 h/day for 6 days and then challenged by inhalation with a minimally irritating concentration of TMA.…”

Section: Toxicity Of Silicamentioning

confidence: 99%

“…When an additional group of animals was exposed to nanosilica before a second challenge to TMA, the pulmonary eosinophilic infiltrate and edema induced by a second TMA challenge in control animals was diminished by the preceding silica exposure, but the number of lymphocytes in the BALF was increased. The authors concluded that SNPs could reduce as well as aggravate certain aspects of TMA-induced respiratory allergy [153]. …”

Section: Toxicity Of Silicamentioning

confidence: 99%

The nanosilica hazard: another variable entity

et al. 2010

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Silica nanoparticles (SNPs) are produced on an industrial scale and are an addition to a growing number of commercial products. SNPs also have great potential for a variety of diagnostic and therapeutic applications in medicine. Contrary to the well-studied crystalline micron-sized silica, relatively little information exists on the toxicity of its amorphous and nano-size forms. Because nanoparticles possess novel properties, kinetics and unusual bioactivity, their potential biological effects may differ greatly from those of micron-size bulk materials. In this review, we summarize the physico-chemical properties of the different nano-sized silica materials that can affect their interaction with biological systems, with a specific emphasis on inhalation exposure. We discuss recent in vitro and in vivo investigations into the toxicity of nanosilica, both crystalline and amorphous. Most of the in vitro studies of SNPs report results of cellular uptake, size- and dose-dependent cytotoxicity, increased reactive oxygen species levels and pro-inflammatory stimulation. Evidence from a limited number of in vivo studies demonstrates largely reversible lung inflammation, granuloma formation and focal emphysema, with no progressive lung fibrosis. Clearly, more research with standardized materials is needed to enable comparison of experimental data for the different forms of nanosilicas and to establish which physico-chemical properties are responsible for the observed toxicity of SNPs.

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“…In contrast, synthetic amorphous silica particles are thought to be much less toxic to the lung. Inhalation of engineered amorphous silica causes only minimal and transient pulmonary inflammation in laboratory rodents [11,12] and no fibrosis of the lungs [13,14] as compared to crystalline silica particles. Few toxicology studies have been conducted to examine the adverse effects of inhaled amorphous SNP and, to the best of our knowledge, no studies have been designed to investigate the potential of these NP to act as adjuvants to enhance the development or exacerbation of allergic airway disease.…”

Section: Introductionmentioning

confidence: 99%

Engineered silica nanoparticles act as adjuvants to enhance allergic airway disease in mice

et al. 2013

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BackgroundWith the increase in production and use of engineered nanoparticles (NP; ≤ 100 nm), safety concerns have risen about the potential health effects of occupational or environmental NP exposure. Results of animal toxicology studies suggest that inhalation of NP may cause pulmonary injury with subsequent acute or chronic inflammation. People with chronic respiratory diseases like asthma or allergic rhinitis may be even more susceptible to toxic effects of inhaled NP. Few studies, however, have investigated adverse effects of inhaled NP that may enhance the development of allergic airway disease.MethodsWe investigated the potential of polyethylene glycol coated amorphous silica NP (SNP; 90 nm diameter) to promote allergic airway disease when co-exposed during sensitization with an allergen. BALB/c mice were sensitized by intranasal instillation with 0.02% ovalbumin (OVA; allergen) or saline (control), and co-exposed to 0, 10, 100, or 400 μg of SNP. OVA-sensitized mice were then challenged intranasally with 0.5% OVA 14 and 15 days after sensitization, and all animals were sacrificed a day after the last OVA challenge. Blood and bronchoalveolar lavage fluid (BALF) were collected, and pulmonary tissue was processed for histopathology and biochemical and molecular analyses.ResultsCo-exposure to SNP during OVA sensitization caused a dose-dependent enhancement of allergic airway disease upon challenge with OVA alone. This adjuvant-like effect was manifested by significantly greater OVA-specific serum IgE, airway eosinophil infiltration, mucous cell metaplasia, and Th2 and Th17 cytokine gene and protein expression, as compared to mice that were sensitized to OVA without SNP. In saline controls, SNP exposure did cause a moderate increase in airway neutrophils at the highest doses.ConclusionsThese results suggest that airway exposure to engineered SNP could enhance allergen sensitization and foster greater manifestation of allergic airway disease upon secondary allergen exposures. Whereas SNP caused innate immune responses at high doses in non-allergic mice, the adjuvant effects of SNP were found at lower doses in allergic mice and were Th2/Th17 related. In conclusion, these findings in mice suggest that individuals exposed to SNP might be more prone to manifest allergic airway disease, due to adjuvant-like properties of SNP.

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Preexposure to Amorphous Silica Particles Attenuates but also Enhances Allergic Reactions in Trimellitic Anhydride-Sensitized Brown Norway Rats

Cited by 9 publications

References 46 publications

Pre-exposure to sulfur dioxide attenuates most allergic reactions upon trimellitic anhydride challenge in sensitized Brown Norway rats

Pre-exposure to sulfur dioxide attenuates most allergic reactions upon trimellitic anhydride challenge in sensitized Brown Norway rats

The nanosilica hazard: another variable entity

Engineered silica nanoparticles act as adjuvants to enhance allergic airway disease in mice

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