There is a growing attention regarding the toxic effect of microplastics pollutants. However, comprehensive phenotyping- and omics-based strategies for the toxicity evaluation of microplastics on the host remain to be established. To this end, we designed an encompassing phenotyping and multi-omics analysis method to detect the molecular interference of nanopolystyrene (PS)-exposed mice. The exposure time was 28 days with 1000 μg/L PS. We found that PS induced microbial alteration and metabolic disorders, which was closely related to immune disturbances. In addition, the altered expression of some genes related to immune dysregulation was observed. Interestingly, Bifidobacterium breve M-16V (B. breve M-16V) significantly inhibited Th2 and Th17 lymphocyte subset. Simultaneously, B.breve M-16V may activate MyD88 expression and promote Th1-related cytokine IL-12 production. In addition, B. breve M-16V may partially restore the gut microbiota dysbiosis. In summary, we demonstrated that the combined phenotyping and omics-based profiling established a practical framework that allowed us to gain a deeper understanding of the maladaptive consequences of PS exposure. It can be utilized to evaluate the toxicity of other environmental microplastics pollutants. Meanwhile, we found that B. breve M-16V has certain anti-inflammatory and immunomodulatory functions through host-microbiome interactions.

The infection and outbreak of Salmonella typhimurium (S. typhimurium) highlight the need for developing a reliable on-site detection strategy fitting to various settings. However, due to the requirement of specialized instruments and trained personnel, traditional detection methods have to be implemented in laboratories and are not ideal for on-site applications. To achieve a sample-to-answer and field-deployable detection for S. typhimurium, we developed an integrated nucleic acid detection platform combining single-vial of loop-mediated isothermal amplification (LAMP)-clustered regularly interspaced short palindromic repeat (CRISPR)/Cas12a system, portable device and smartphone app. This platform enables the extraction, concentration, and purification of DNA, amplification of the target, and output of visual fluorescent signals within 1 h. With this detection platform, 10² CFU/mL of S. typhimurium in food and environmental matrix was able to be accurately detected. This method demonstrated excellent selectivity. Also, an auxiliary smartphone application was developed to achieve simplified result interpretation. Our method exhibited potential to better control and respond to outbreaks of foodborne diseases, especially in low-resource settings.

Methylmercury (MeHg) is a global environmental pollutant with neurotoxicity, which can easily crosses the blood-brain barrier and cause irreversible damage to the human central nervous system (CNS). CNS inflammation and autophagy are known to be involved in the pathology of neurodegenerative diseases. Meanwhile, MeHg has the potential to induce microglia-mediated neuroinflammation as well as autophagy. This study aims to further explore the exact molecular mechanism of MeHg neurotoxicity. We conducted in vitro studies using BV2 microglial cell from the central nervous system of mice. The role of inflammation and autophagy in the damage of BV2 cells induced by MeHg was determined by detecting cell viability, cell morphology and structure, reactive oxygen species (ROS), antioxidant function, inflammatory factors, autophagosomes, inflammation and autophagy-related proteins. We further investigated the relationship between the inflammatory response and autophagy induced by MeHg by inhibiting them separately. The results indicated that MeHg could invade cells, change cell structure, activate NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome and autophagosome, release a large amount of inflammatory factors and trigger the inflammatory response and autophagy. It was also found that MeHg could disrupt the antioxidant function of cells. In addition, the inhibition of NLRP3 inflammasome alleviated both cellular inflammation and autophagy, while inhibition of autophagy increased cellular inflammation. Our current research suggests that MeHg might induce BV2 cytotoxicity through inflammatory response and autophagy, which may be mediated by the NLRP3 inflammasome activated by oxidative stress.

Background and Objective: Oxidative stress is an important pathological process in ischemic stroke (IS). Apigenin (APG) is a natural product with favorable antioxidative effects, and some studies have already demonstrated the antioxidative mechanism of APG in the treatment of IS. However, the mechanism of APG on DNA damage and repair after IS is not clear. The aim of this study was to investigate the mechanism of APG on DNA repair after IS.Methods: Male Sprague-Dawley rats were used to establish a model of permanent middle cerebral artery occlusion (pMCAO) on one side, and were pre-treated with gavage of APG (30, 60, or 120 mg/kg) for 7 days. One day after pMCAO, the brain tissues were collected. Cerebral infarct volume, brain water content, HE staining and antioxidant index were analyzed to evaluated the brain damage. Molecular Docking, molecular dynamics (MD) simulation, immunohistochemistry, and Western blot were used to explore the potential proteins related to DNA damage repair.Results: APG has a low binding score with DNA repair-related proteins. APG treatment has improved the volume of cerebral infarction and neurological deficits, reduced brain edema, and decreased parthanatos and apoptosis by inhibiting PARP1/AIF pathway. In addition, APG improved the antioxidative capacity through reducing reactive oxygen species and malondialdehyde, and increasing glutathione and superoxide dismutase. Also, APG has reduced DNA damage- and cell death-related proteins such as PARP1, γH2A.X, 53BP1, AIF, cleaved caspase3, Cytochrome c, and increased DNA repair by BRCA1 and RAD51 through homologous recombination repair, and reduced non-homologous end link repair by KU70.Conclusion: APG can improve nerve damage after IS, and these protective effects were realized by reducing oxidative stress and DNA damage, and improving DNA repair.