Deciphering the interplay between LPS/TLR4 pathways, neurotransmitter, and deltamethrin-induced depressive-like behavior: Perspectives from the gut-brain axis.

The improper use of deltamethrin (DM) can result in its accumulation in soil, water, food, and even the human body, which is associated with an elevated risk of neurotoxicity and behavioral abnormalities; however, the underlying mechanisms remain insufficiently investigated. Emerging evidence underscores the significance of the gut-brain axis in central nervous system (CNS) dysfunctions. Accordingly, this study investigates the role of the gut-brain axis in DM-induced behavioral anomalies in mice. The results showed that DM exposure induced depressive-like behavior, and the hippocampus, the region that is responsible for the modulation of emotional behavior, showed structural integrity disrupted (neuronal nuclear shrinkage and decreased tight junction protein expression). In addition, DM exposure led to compromised gut barrier integrity (disruptions on crypt surfaces and decreased tight junction protein expression), which might contribute to the gut bacterial-derived lipopolysaccharide (LPS) leakage into the bloodstream and reaching the brain, triggering LPS/toll-like receptor (TLR) 4 -mediated increases in brain pro-inflammatory cytokines. Subsequently, we observed a disturbance in neurotransmitter metabolic pathways following DM exposure, which inhibited the production of 5-hydroxytryptamine (5-HT). Additionally, DM exposure resulted in gut microbiota dysbiosis. Characteristic bacteria, such as Alistipes, Bifidobacterium, Gram-negative bacterium cTPY-13, and Odoribacter exhibited significant correlations with behavior, tight junction proteins, inflammatory response, and neurotransmitters. Further fecal microbiota transplantation (FMT) experiments suggested that DM-induced gut microbiota dysbiosis might contribute to depressive-like behavior. These results provide a new perspective on the toxicity mechanism of DM, indicating that its neurotoxicity may be partially regulated by the microbiota-gut-brain axis.

Heterodyne laser Doppler vibrometer with squeezed light enhancement.

An important feature of a heterodyne laser Doppler vibrometer (LDV) is the possibility of measuring an optical path length oscillation at a frequency f at a choosable frequency fhet ± f, at which the photo-electric measurement shows an optical quantum noise that is significantly greater than the detector dark noise. The full-squeezed light enhancement of a heterodyne LDV's signal-to-noise ratio has not been achieved so far. Here we use a sideband spectrum that is squeezed around fhet = 40 MHz and demonstrate the squeezing-enhanced measurement of an optical path length vibration at f = 1 MHz of about 3.5 dB while fully maintaining the signal power. The proof of principle we provide will enable the realization of ultra-precise LDVs over an extended signal bandwidth for probes or environments that require low intensities.

Multiple perspectives reveal the gut toxicity of polystyrene microplastics on Eisenia fetida: Insights into community signatures of gut bacteria and their translocation.

The gut is the primary pathway by which soil animals are exposed to microplastics (MPs). However, the gut toxicity of MPs has not been elucidated in earthworms. Herein, we aimed to study the gut toxicity (e.g., gut barrier dysfunction, gut bacterial translocation, and pathogen invasion) of polystyrene microplastics (PS-MPs) on Eisenia fetida and its relationship with gut bacteria. We found that PS-MPs exposure caused gut barrier damage to Eisenia fetida. This damage included apparent injury of gut epithelial cells and significantly lower transcription levels of genes coding for gut tight junction (TJ)-related proteins. We then observed significantly increased levels of bacterial lipopolysaccharide (LPS) and gut bacterial load, indicating the occurrence of gut bacterial translocation and related barrier damage. Subsequently, antibacterial immune responses were activated and accompanied by a failure of the antioxidant defense system, indicating that pathogen invasion might occur. Gut barrier damage could weaken host selective pressures (deterministic process) on gut bacteria, such as particular pathogens. Indeed, members of Proteobacteria, e.g., Aeromonas and Escherichia/Shigella, regarded as potential opportunistic pathogens, were remarkable signatures of groups exposed to PS-MPs. These potential opportunistic gut bacteria were pivotal contributors to gut TJ damage and gut bacterial translocation resulting from PS-MPs exposure. In addition, the gut bacterial networks of PS-MPs exposure groups were more uncomplicated than those of the control group, but more negative interactions were easy to observe. In conclusion, our work sheds light on the molecular mechanism of earthworm gut toxicity caused by PS-MPs exposure and provides a prospective risk assessment of MPs in soil ecosystems.