Abstract
Engineered nanomaterials (ENMs) are products of the emerging nanotechnology industry and many different types of ENMs have been shown to cause chronic inflammation in the lungs of rodents after inhalation exposure, suggesting a risk to human health. Due to the increasing demand and use of ENMs in a variety of products, a careful evaluation of the risks to human health is urgently needed. An assessment of the immunotoxicity of ENMs should consider susceptibility factors including sex, pre-existing diseases, deficiency of specific genes encoding proteins involved in the innate or adaptive immune response, and co-exposures to other chemicals. This review will address evidence from experimental animal models that highlights some important issues of susceptibility to chronic lung inflammation and systemic immune dysfunction after pulmonary exposure to ENMs.
Highlights
Inflammation is the consequence of an innate immune response of the host to stimuli such as pathogens, allergens, or toxic chemicals and pollutants [1,2,3]
Since T-bet KO mice are susceptible to chronic allergic lung inflammation caused by nickel nanoparticles (NiNPs) and multi-walled carbon nanotubes (MWCNTs), this suggests that individuals with T-bet deficiency would be more susceptible to certain types of Engineered nanomaterials (ENMs)
The results suggest that the impaired resolution of the inflammatory response may develop into a chronic unresolved inflammatory state, due to prolonged increase in neutrophils and pro-inflammatory cytokines, in NADPH oxidase deficient mice [102]
Summary
Inflammation is the consequence of an innate immune response of the host to stimuli such as pathogens (e.g., bacteria, fungi, viruses), allergens, or toxic chemicals and pollutants [1,2,3]. Since T-bet KO mice are susceptible to chronic allergic lung inflammation caused by NiNPs and MWCNTs, this suggests that individuals with T-bet deficiency would be more susceptible to certain types of ENMs. Nuclear factor erythroid 2-related factor (Nrf2) is a transcription factor that controls the expression of antioxidant proteins [88]. Exposure of Nrf KO mice to MWCNTs by oropharyngeal aspiration showed a higher level of inflammation and fibrosis with increased inflammatory cell infiltrates in the lungs 7 days after the initial exposure compared to the wild type mice [90]. P53 could play a role in suppressing chronic lung inflammation and granuloma formation upon pulmonary exposures to different ENMs, including SWCNTs and MWCNTs. Deficiency of p53 in experimental animals and humans is a susceptibility factor in pulmonary diseases, including cancer and pulmonary fibrosis. 6.4 or 25.6 μg via oropharyngeal aspiration 6.4 or 12.8 μg via oropharyngeal aspiration
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