Surface PEGylation Suppresses Pulmonary Effects of CuO in Allergen-Induced Lung Inflammation
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ABSTRACT:
PROVIDER: PRJNA503901 | ENA |
REPOSITORIES: ENA
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Project description:The objective of the study was to investigate how pristine CuO modulates allergic lung inflammation and whether surface modifications can influence its reactivity. CuO materials exacerbated the existing allergic airway inflammation by eliciting dramatic pulmonary neutrophilia. Transcriptomic analysis showed that CuO, CuO COOH and CuO NH3 commonly enriched neutrophil-related biological processes in lungs with and without the pre-existing condition. In contrast, CuO PEG had a significantly lower potential in triggering pulmonary changes revealing that surface PEGylation suppresses the effects triggered by the pristine material.
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Project description:This study investigated the pulmonary toxicity of Copper oxide nanoparticles (CuO NPs) surface modified with polyethylenimine (PEI) or ascorbate (ASC), was investigated. Rats were exposed nose-only to a fixed exposure concentration of ASC or PEI coated CuO NPs for 5 consecutive days. On day 6 and day 27 post-exposure, pulmonary toxicity markers in bronchoalveolar lavage fluid (BALF) were analyzed and histopathological evaluation of the lungs was performed, along with microarray analyses on whole lung tissue samples.
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Project description:BACKGROUND:Copper oxide (CuO) nanomaterials are used in a wide range of industrial and commercial applications. These materials can be hazardous, especially if they are inhaled. As a result, the pulmonary effects of CuO nanomaterials have been studied in healthy subjects but limited knowledge exists today about their effects on lungs with allergic airway inflammation (AAI). The objective of this study was to investigate how pristine CuO modulates allergic lung inflammation and whether surface modifications can influence its reactivity. CuO and its carboxylated (CuO COOH), methylaminated (CuO NH3) and PEGylated (CuO PEG) derivatives were administered here on four consecutive days via oropharyngeal aspiration in a mouse model of AAI. Standard genome-wide gene expression profiling as well as conventional histopathological and immunological methods were used to investigate the modulatory effects of the nanomaterials on both healthy and compromised immune system. RESULTS:Our data demonstrates that although CuO materials did not considerably influence hallmarks of allergic airway inflammation, the materials exacerbated the existing lung inflammation by eliciting dramatic pulmonary neutrophilia. Transcriptomic analysis showed that CuO, CuO COOH and CuO NH3 commonly enriched neutrophil-related biological processes, especially in healthy mice. In sharp contrast, CuO PEG had a significantly lower potential in triggering changes in lungs of healthy and allergic mice revealing that surface PEGylation suppresses the effects triggered by the pristine material. CONCLUSIONS:CuO as well as its functionalized forms worsen allergic airway inflammation by causing neutrophilia in the lungs, however, our results also show that surface PEGylation can be a promising approach for inhibiting the effects of pristine CuO. Our study provides information for health and safety assessment of modified CuO materials, and it can be useful in the development of nanomedical applications.
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