Browse Articles

Innovative approach for experimental investigation and monitoring and warning of the evolutionary patterns of dam body failure in earth dams

Coxiella burnetii manipulates the lysosomal protease cathepsin B to facilitate intracellular success

Abstract The obligate intracellular bacterium Coxiella burnetii establishes an intracellular replicative niche termed the Coxiella-containing vacuole (CCV), which has been characterised as a bacterially modified phagolysosome. How C. burnetii withstands the acidic and degradative properties of this compartment is not well understood. We demonstrate that the key lysosomal protease cathepsin B is actively and selectively removed from C. burnetii-infected cells through a mechanism involving the Dot/Icm type IV-B secretion system effector CvpB. Overexpression of cathepsin B leads to defects in CCV biogenesis and bacterial replication, indicating that removal of this protein represents a strategy to reduce the hostility of the intracellular niche. In addition, we show that C. burnetii infection of mammalian cells induces the secretion of a wider cohort of lysosomal proteins, including cathepsin B, to the extracellular milieu via a mechanism dependent on retrograde traffic. This study reveals that C. burnetii is actively modulating the hydrolase cohort of its replicative niche to promote intracellular success and demonstrates that infection incites the secretory pathway to maintain lysosomal homoeostasis.

Anti-inflammatory effects of 64Zn-aspartate is accompanied by cognitive improvements in rats with Aβ1-40-induced alzheimer disease

mRNA technology helps reinvigorate the hunt for cancer vaccines

Overcoming lattice mismatch for core-shell NaGdF4@CsPbBr3 heterostructures

Allicin and hesperidin protect sperm production from environmental toxins in mice

Cryo-EM captures the coordination of asymmetric electron transfer through a di-copper site in DPOR

Systemic inflammation accelerates the development of focal segmental glomerulosclerosis in a mouse model of adriamycin induced nephrosis

Neural representation of cytokines by vagal sensory neurons

Abstract The nervous system coordinates with the immune system to detect and respond to harmful stimuli. Inflammation is a universal response to injury and infection that involves the release of cytokines. While it is known that information about cytokines is transmitted from the body to the brain, how the nervous system encodes specific cytokines in the form of neural activity is not well understood. Using in vivo calcium imaging, we show that vagal sensory neurons within the nodose ganglia exhibit distinct real-time neuronal responses to inflammatory cytokines. Some neurons respond selectively to individual cytokines, while others encode multiple cytokines with distinct activity patterns. In male mice with induced colitis, inflammation increased the baseline activity of these neurons but decreased responsiveness to specific cytokines, reflecting altered neural excitability. Transcriptomic analysis of vagal ganglia from colitis mice revealed downregulation of cytokine signaling pathways, while neuronal activity pathways were upregulated. Thus, nodose ganglia neurons perform real-time encoding of cytokines at the first neural station in a body-brain axis, providing a new framework for studying the dynamic nature of neuroimmune communication.

FG-4592 combined with PRP significantly accelerates the healing of refractory diabetic wounds by upregulating HIF-1α

Long-distance coherent quantum communications in deployed telecom networks

Norway set to scrap mandatory language training for foreign postdocs and PhD students

Experimental determination of giant polarization in wurtzite III-nitride semiconductors

The relationship between the ratio of triglyceride to high-density lipoprotein cholesterol and left ventricular hypertrophy in Chinese hypertension adults

Comparative characterization of human accelerated regions in neurons

Human V4 size predicts crowding distance

Self-determination, motivation and burnout among residents in Lebanon

Regulating Na content and Mn defects in birnessite for high-voltage aqueous sodium-ion batteries

Exploring hypoxia driven subtypes of pulmonary arterial hypertension through transcriptomics single cell sequencing and machine learning

A hypothalamic circuit underlying the dynamic control of social homeostasis

Abstract Social grouping increases survival in many species, including humans 1,2 . By contrast, social isolation generates an aversive state (‘loneliness’) that motivates social seeking and heightens social interaction upon reunion 3–5 . The observed rebound in social interaction triggered by isolation suggests a homeostatic process underlying the control of social need, similar to physiological drives such as hunger, thirst or sleep 3,6 . In this study, we assessed social responses in several mouse strains, among which FVB/NJ mice emerged as highly, and C57BL/6J mice as moderately, sensitive to social isolation. Using both strains, we uncovered two previously uncharacterized neuronal populations in the hypothalamic preoptic nucleus that are activated during either social isolation or social rebound and orchestrate the behaviour display of social need and social satiety, respectively. We identified direct connectivity between these two populations and with brain areas associated with social behaviour, emotional state, reward and physiological needs and showed that mice require touch to assess the presence of others and fulfil their social need. These data show a brain-wide neural system underlying social homeostasis and provide significant mechanistic insights into the nature and function of circuits controlling instinctive social need and for the understanding of healthy and diseased brain states associated with social context.