Enhanced silver nanoparticle-induced pulmonary inflammation in a metabolic syndrome mouse model and resolvin D1 treatment

Abstract

Background Metabolic syndrome (MetS) exacerbates susceptibility to inhalation exposures such as particulate air pollution, however, the mechanisms responsible remain unelucidated. Previously, we determined a MetS mouse model exhibited exacerbated pulmonary inflammation 24 h following AgNP exposure compared to a healthy mouse model. This enhanced response corresponded with reduction of distinct resolution mediators. We hypothesized silver nanoparticle (AgNP) exposure in MetS results in sustained pulmonary inflammation. Further, we hypothesized treatment with resolvin D1 (RvD1) will reduce exacerbations in AgNP-induced inflammation due to MetS. Results To evaluate these hypotheses, healthy and MetS mouse models were exposed to vehicle (control) or AgNPs and a day later, treated with resolvin D1 (RvD1) or vehicle (control) via oropharyngeal aspiration. Pulmonary lung toxicity was evaluated at 3-, 7-, 14-, and 21-days following AgNP exposure. MetS mice exposed to AgNPs and receiving vehicle treatment, demonstrated exacerbated pulmonary inflammatory responses compared to healthy mice. In the AgNP exposed mice receiving RvD1, pulmonary inflammatory response in MetS was reduced to levels comparable to healthy mice exposed to AgNPs. This included decreases in neutrophil influx and inflammatory cytokines, as well as elevated anti-inflammatory cytokines. Conclusions Inefficient resolution may contribute to enhancements in MetS susceptibility to AgNP exposure causing an increased pulmonary inflammatory response. Treatments utilizing specific resolution mediators may be beneficial to individuals suffering MetS following inhalation exposures.

Monocyte (THP-1) Response to Silver Nanoparticles Synthesized with Rumex hymenosepalus Root Extract

“…Other investigations with the THP-1 monocytic cell line showed no induction of IL-4 production by AgNPs obtained through the reduction of silver nitrate with sodium borohydride [ 85 ]. Furthermore, it was observed that IL-4 production decreased in the lungs of mice that were chronically exposed to AgNPs and had metabolic syndrome [ 86 ].…”

Transcriptomic Profiling the Effects of Airway Exposure of Zinc Oxide and Silver Nanoparticles in Mouse Lungs

“…A pathway analysis of 670 ± 49 ng/cm 2 aerosol nAg (14.1 ± 2.3 nm) inhalation exposure to rats after 1 or 7 days enriched the same pathways related to granulocyte and agranulocyte adhesion and diapedesis, IL-10 signaling and hypercytokinemia [ 43 ]. Another study found that 50 μg (20 nm) citrate-coated nAg exposure to mice elevated IL-4 and IL-10 gene expression after 7 days [ 44 ]. Additionally, a study using an in vitro alveolar model composed of an alveolar type-II cell line (A549), differentiated macrophage-like cells (THP-1), mast cells (HMC-1), and endothelial cells (EA.Hy926) found that 0.5 and 5 μg/cm 2 PVP-coated nAg (50 nm) increased the secretion of IL-4, IL-6, and IL-10 after 6 h and 24 h [ 45 ].…”

Toxicological impact of microplastics and nanoplastics on humans: understanding the mechanistic aspect of the interaction

“…In disease environments, including conditions like metabolic syndrome tied to lipid dysregulation, the constitution of macromolecules differs from that in healthy scenarios. Interestingly, it has been observed that the corona around silver nanoparticles in a metabolic syndrome environment can exacerbate inflammatory responses in mice exhibiting metabolic syndromes compared to their healthy counterparts (Alqahtani et al, 2020;Kobos et al, 2020;Alqahtani et al, 2021;Alqahtani et al, 2022). NPs can be transported and internalized into cells either passively or actively.…”