Biology subjects

Wang, H.-B.

Publications and source records attributed to Wang, H.-B..

6 recordsLinked to original sources

bioRxiv2025

Identification of Vector Organisms and Their Carried Pathogens by Metagenomic Sequencing

Vector surveillance is vital for public health, yet traditional methods often face limitations. This study assessed the use of metagenomic sequencing for analyzing mosquitoes, cockroaches, flies, and rodents from Zhongshan, China. The results revealed a high concordance between metagenomic and Sanger sequencing for species identification (Kappa = 0.667, P = 0.011). Metagenomic analysis identified vector-specific dominant bacteria, including Wolbachia in mosquitoes, Blattabacterium sp. in cockroaches, Bartonella tribocorum and Leptospira interrogans in rodents, and Vagococcus teuberi in flies. It also detected numerous classical pathogens, such as Enterococcus faecalis, L. interrogans, and Klebsiella pneumoniae. Among the identified fungi and viruses, 19 were human pathogens, while seven posed a threat to agriculture, notably Pepper mild mottle virus and Tomato brown rugose fruit virus. These findings systematically characterize the microbial communities associated with various vectors, highlight the potential of metagenomics for broad pathogen screening, and underscore its utility in large-scale vector surveillance and public health protection. ImportanceVectors are major carriers of numerous diseases and present risks fot cross-border transmission. Existing detection methods for vectors and their pathogens remain inefficient, insensitive, and prone to difficulties in species identification. Despite extensive efforts in vector identification, the potential threats posed by their associated pathogens remain unclear, demonstrating the need for more effective diagnostic strategies. Metagenomic sequencing offers a promising solution to this challenge. In this study, we applied metagenomic sequencing to vectors collected from urban and port areas in Zhongshan, China, to evaluate its efficacy in pathogen detection. Overall, our work contributes to a better understanding of the public health risks posed by vector-borne pathogens.

microbiology↗

bioRxiv2025

Dissociating the Effects of Light at Night from Circadian Misalignment in a Neurodevelopmental Disorder Mouse Model Using Ultradian Light-Dark Cycles.

Individuals with neurodevelopmental disorders (NDDs) often experience sleep disturbances and are frequently exposed to light during nighttime hours. Our previous studies using the Cntnap2 knockout (KO) mouse model of NDDs demonstrated that nighttime light exposure increases behaviors such as excessive grooming, reduces social interactions, and disrupts daily locomotor rhythms. To further evaluate the effects of nighttime light exposure, we exposed wild-type (WT) and Cntnap2 KO mice to an ultradian lighting cycle (T7), which alternates 3.5 hours of light and 3.5 hours of darkness. Circadian rhythms in activity, corticosterone levels, and clock gene expression are maintained under T7 lighting despite the presence of light during the usual night phase, whilst animals display increased depressive-like behaviors and reduce performance on the novel object recognition test. Based on these observations, we hypothesized that T7 lighting would mimic the impact of nighttime light exposure seen in standard light-dark cycles with dim light at night (DLaN). However, in this study, adult WT and Cntnap2 KO mice held under the T7 cycle did not show the increased grooming behavior or reduced social interaction observed in Cntnap2 KO mice exposed to DLaN. Regarding locomotor activity rhythms, the T7 cycle lengthened the circadian period and weakened the rhythm amplitude but did not abolish rhythmicity in either genotype. Finally, opposite to DLaN, neither the T7 cycle nor constant darkness (DD) elicited an increase in cFos expression in the basolateral amygdala in WT and KO mice. These results demonstrate that the adverse behavioral and neurobiological effects of nighttime light exposure in a model of a neurodevelopmental disorder depend on circadian disruption rather than light exposure alone, highlighting the importance of circadian stability as a protective factor in NDDS.

neuroscience↗

bioRxiv2024

Scheduled feeding improves behavioral outcomes and reduces inflammation in a mouse model of Fragile X syndrome.

Fragile X syndrome (FXS), a leading inherited cause of intellectual disability and autism, is frequently accompanied by sleep and circadian rhythm disturbances. In this study, we comprehensively characterized these disruptions and evaluated the therapeutic potential of a circadian-based intervention in the fragile X mental retardation 1 (FMR1) knockout (KO) mouse. The Fmr1 KO mice exhibited fragmented sleep, impaired locomotor rhythmicity, and attenuated behavioral responses to light, linked to an abnormal retinal innervation and reduction of light-evoked neuronal activation in the suprachiasmatic nucleus. Behavioral testing revealed significant deficits in social memory and increased repetitive behaviors in the mutants, which correlated with sleep fragmentation. Remarkably, a scheduled feeding paradigm (6-hour feeding/18-hour fasting) significantly enhanced circadian rhythmicity, consolidated sleep, and improved social deficits and repetitive behaviors in the Fmr1 KO mice. This intervention also normalized the elevated levels of some pro-inflammatory cytokines, including IL-12 and IFN-{gamma}, in the mutants blood, suggesting that its benefits extend to inflammatory pathways. These findings highlight the interplay between circadian disruption, behavior, and an inflammatory response in FXS, and provide compelling evidence that time-restricted feeding may serve as a promising non-pharmacological approach for improving core symptoms in neurodevelopmental disorders.

neuroscience↗

bioRxiv2022

Long wavelength light reduces the negative consequences of dim light at night in the Cntnap2 mouse model of autism.

Many patients with autism spectrum disorders (ASD) show disturbances in their sleep/wake cycles, and may be particularly vulnerable to the impact of circadian disruptors. We have previously shown that exposure to dim light at night (DLaN) in contactin associated protein-like 2 knock out (Cntnap2 KO) mice disrupts diurnal rhythms, increases repetitive behaviors while reducing social interactions. These negative effects of DLaN may be mediated by intrinsically photosensitive retinal ganglion cells (ipRGCs) expressing the photopigment melanopsin, which is maximally sensitive to blue light (480nm). In this study, we used a light-emitting diode (LED) array that enabled us to shift the spectral properties of the DLaN while keeping the intensity at 10 lx. First, using wild-type (WT) mice, we confirmed that the short-wavelength enriched lighting produced strong acute suppression of locomotor activity (masking), robust light-induced phase shifts, and c-Fos expression in the suprachiasmatic nucleus, while the long-wavelength enriched lighting evoked much weaker responses. Furthermore, exposure of WT mice to the short-wavelength light at night reduced the amplitude of locomotor activity rhythms and impaired social interactions. Mice lacking the melanopsin expressing ipRGCs (Opn4DTA mice) were resistant to these negative effects of DLaN. Importantly, the shift of the DLaN stimulus to longer wavelengths ameliorated the negative impact on the activity rhythms and autistic behaviors (i.e. reciprocal social interactions, repetitive grooming) of the Cntnap2 KO model. The short-, but not the long-wavelength enriched, DLaN triggered cFos expression in the peri-habenula region as well as in the basolateral amygdala (BLA). Finally, DLaN-driven c-Fos induction in BLA glutamatergic neurons was about 3-fold higher in the Cntnap2 KO mice, suggesting that these cells may be particularly vulnerable to the effects of photic disruption. Broadly, our findings suggest that the spectral properties of light at night should be considered in the management of ASD and other neurodevelopmental disorders.

neuroscience↗

bioRxiv2021

Maternal Ezh1/2 deficiency in oocyte delays H3K27me2/3 restoration and impairs epiblast development responsible for embryonic sub-lethality in mouse

Mammalian embryonic development is a complex process regulated by various epigenetic modifications. Recently, maternal histone H3 methylations were found to be inherited and reprogrammed in early embryos to regulate embryonic development. The enhancer of zest homolog 1 and 2 (Ezh1 and Ezh2) belong to the core components of Polycomb repressive complex 2 (PRC2) and are the histone methyltransferase of histone 3 lysine 27 (H3K27). How maternal Ezh1 and Ezh2 function on H3K27 methylation in in vivo preimplantation embryos and embryonic development are not clear. Here, we deleted Ezh1 or/and Ezh2 in growing oocytes using gene knockout mouse models, and found that H3K27me3 in oocytes was disappeared by loss of Ezh2 alone while H3K27me2 was absent upon deletion of both Ezh1 and Ezh2. The effects of Ezh1/2 were inherited in maternal knockout zygotes and early embryos, in which restoration of H3K27me3 was delayed until late blastocyte by loss of Ezh2 alone and H3K27me2 was reestablished until morulae by deletion of Ezh1 and Ezh2. However, the ablation of both Ezh1 and Ezh2, but not single Ezh1 or Ezh2, led to significantly decreased litter size due to growth retardation during post-implantation. Furthermore, maternal Ezh1/2 deficiency caused compromised H3K27me3 and pluripotent epiblast cells in late blastocyst, followed by defective development of epiblast. These results demonstrate that in oocytes, Ezh2 is indispensable for H3K27me3 while Ezh1 complements Ezh2 in H3K27me2. Also, maternal Ezh1/2-H3K27 methylation is inherited in descendant embryos and has a critical effect on fetus and placenta development. Thus, this work sheds light on maternal epigenetic modifications during embryonic development.

developmental biology↗

bioRxiv2020

Longitudinal single-cell immune profiling revealed distinct innate immune response in asymptomatic COVID-19 patients

Recent studies have characterized the single-cell immune landscape of host immune response of coronavirus disease 2019 (COVID-19), specifically focus on the severe condition. However, the immune response in mild or even asymptomatic patients remains unclear. Here, we performed longitudinal single-cell transcriptome sequencing and T cell/B cell receptor sequencing on 3 healthy donors and 10 COVID-19 patients with asymptomatic, moderate, and severe conditions. We found asymptomatic patients displayed distinct innate immune responses, including increased CD56briCD16- NK subset, which was nearly missing in severe condition and enrichment of a new Th2-like cell type/state expressing a ciliated cell marker. Unlike that in moderate condition, asymptomatic patients lacked clonal expansion of effector CD8+ T cells but had a robust effector CD4+ T cell clonal expansion, coincide with previously detected SARS-CoV-2-reactive CD4+ T cells in unexposed individuals. Moreover, NK and effector T cells in asymptomatic patients have upregulated cytokine related genes, such as IFNG and XCL2. Our data suggest early innate immune response and type I immunity may contribute to the asymptomatic phenotype in COVID-19 disease, which could in turn deepen our understanding of severe COVID-19 and guide early prediction and therapeutics.

immunology↗