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Fe3O4 Nanoparticles Attenuated Salmonella Infection in Chicken Liver Through Reactive Oxygen and Autophagy via PI3K/Akt/mTOR Signaling.

ABSTRACT: Recently nanomaterials have received substantial attention in biotechnology areas for their innovative properties in physical and chemical function. One of the most arrestive properties of nanomaterials that has been reported is their bacteriostatic activity. Our previous research found that Fe3O4 magnetic nanoparticles (Fe3O4-NPs) could effectively reduce the viability of intracellular Salmonella Enteritidis in chicken cells. There is an essential need to explore whether the bacteriostatic activity of Fe3O4-NPs is available in vivo. As an extension of this research, we conducted the present study to investigate the potential effect of Fe3O4-NPs used for S. Enteritidis control in chickens and to extensively investigate the underlying mechanisms in the process. The overall study included the evaluation of pathological sections, antioxidant status, inflammation, and the autophagy status of chicken liver, including the signaling pathway involved in the process. Results indicated that Fe3O4-NPs pretreatment can effectively inhibit the invasion of S. Enteritidis in chicken liver. Fe3O4-NPs pretreatment significantly increased reactive oxygen species (ROS) generation in chickens, including antioxidant enzyme activities. S. Enteritidis infection significantly increased the protein expression of the autophagy marker LC3. Additionally, the inflammation response and pathological changes caused by S. Enteritidis infection were alleviated by Fe3O4-NPs pretreatment. Phosphorylated mTOR was significantly increased in S. Enteritidis infected chickens, but showed no difference in chickens pretreated with Fe3O4-NPs. In summary, the results demonstrated that ROS and autophagy were involved in the inhibition of S. Enteritidis in chickens by Fe3O4-NPs pretreatment. The redox balance and inflammation response appeared normal in the process, as did the expression of the PI3K/Akt/mTOR signaling pathways. Taken together, our research demonstrate that the bacteriostatic activity of Fe3O4-NPs in chickens is avaliable and safe, which can be an alternative to antibiotics for bacterial inhibition in poultry industry.

SUBMITTER: Shen Y

PROVIDER: S-EPMC6978669 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Fe3O4 Nanoparticles Attenuated Salmonella Infection in Chicken Liver Through Reactive Oxygen and Autophagy via PI3K/Akt/mTOR Signaling.

Shen Yiru Y Xiao Yunqi Y Zhang Shan S Wu Shu S Gao Lizeng L Shi Shourong S

Frontiers in physiology 20200117

Recently nanomaterials have received substantial attention in biotechnology areas for their innovative properties in physical and chemical function. One of the most arrestive properties of nanomaterials that has been reported is their bacteriostatic activity. Our previous research found that Fe3O4 magnetic nanoparticles (Fe3O4-NPs) could effectively reduce the viability of intracellular Salmonella Enteritidis in chicken cells. There is an essent ...[more]

PMID: 32009981

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Project description:Environmental exposure to silica nanoparticles (SiNPs) is inevitable due to their widespread application in industrial, commercial, and biomedical fields. In recent years, most investigators focus on the evaluation of cardiovascular effects of SiNPs in vivo and in vitro. Endothelial injury and dysfunction is now hypothesized to be a dominant mechanism in the development of cardiovascular diseases. This study aimed to explore interaction of SiNPs with endothelial cells, and extensively investigate the exact effects of reactive oxygen species (ROS) on the signaling molecules and cytotoxicity involved in SiNPs-induced endothelial injury. Significant induction of cytotoxicity as well as oxidative stress, apoptosis, and autophagy was observed in human umbilical vein endothelial cells following the SiNPs exposure (P<0.05). The oxidative stress was induced by ROS generation, leading to redox imbalance and lipid peroxidation. SiNPs induced mitochondrial dysfunction, characterized by membrane potential collapse, and elevated Bax and declined bcl-2 expression, ultimately leading to apoptosis, and also increased number of autophagosomes and autophagy marker proteins, such as LC3 and p62. Phosphorylated ERK, PI3K, Akt, and mTOR were significantly decreased, but phosphorylated JNK and p38 MAPK were increased in SiNPs-exposed endothelial cells. In contrast, all of these stimulation phenomena were effectively inhibited by N-acetylcysteine. The N-acetylcysteine supplement attenuated SiNPs-induced endothelial toxicity through inhibition of apoptosis and autophagy via MAPK/Bcl-2 and PI3K/Akt/mTOR signaling, as well as suppression of intracellular ROS property via activating antioxidant enzyme and Nrf2 signaling. In summary, the results demonstrated that SiNPs triggered autophagy and apoptosis via ROS-mediated MAPK/Bcl-2 and PI3K/Akt/mTOR signaling in endothelial cells, and subsequently disturbed the endothelial homeostasis and impaired endothelium. Our findings may provide experimental evidence and explanation for cardiovascular diseases triggered by SiNPs. Furthermore, results hint that the application of antioxidant may provide a novel way for safer use of nanomaterials.

Dataset Information

Fe3O4 Nanoparticles Attenuated Salmonella Infection in Chicken Liver Through Reactive Oxygen and Autophagy via PI3K/Akt/mTOR Signaling.

Publications

Fe<sub>3</sub>O<sub>4</sub> Nanoparticles Attenuated <i>Salmonella</i> Infection in Chicken Liver Through Reactive Oxygen and Autophagy via PI3K/Akt/mTOR Signaling.

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