Multi-virulence and phenotypic spread of Campylobacter jejuni carried by chicken meat in Brazil

Campylobacter jejuni is the most incriminated pathogen in bacterial gastroenteritis, and therefore, characteristics of its epidemiology must be continuously investigated to support possible mitigating measures. This is particularly important when evaluating representative strains of the world's leading chicken meat exporter, Brazil. We evaluated a panel of 14 virulence genes in 359 strains of C. jejuni isolated from chilled broiler carcasses of Brazil. The genes were classified into five virulence categories (B: biofilm/motility; SS: secretion/cytotoxicity system; CI: invasion/colonization; GB: Guillain-Barré and AE: adaptation to stress). The percentage of strains with stress adaptation genes (86.07%) indicates the potential to adapt to unfavorable environmental conditions and hcp gene in 97.77%, indicates the ability to cause serious infections in humans. Genes related to GBS in 77.44% of strains are an additional concern, which must be monitored. The gene panel showed the presence of 124 virulence profiles. Individual analyzes by carcass, slaughter establishment, and municipalities where they were located showed high I.Var., of 0.82, 0.87 and 0.78, respectively. Georeferencing indicated state A as a hotspot for virulent strains. Higher levels of isolation and multi-virulence were identified in the summer, which in Brazil is hot and humid. Proteomics was able to discriminate the strains, but due to the high heterogeneity between them, it did not allow to explain their dissemination. Together, our results showed that the studied strains are a potential danger to public health and that there is an urgent need for their surveillance and the adoption of control measures, especially in state A.

GRASPing the unconventional secretory machinery to bridge cellular stress signaling to the extracellular proteome

Cellular adaptation to stress is a crucial homeostatic process for survival, metabolism, physiology, and disease. Cells respond to stress stimuli (e.g., nutrient starvation, growth factor deprivation, hypoxia, low energy, etc.) by changing the activity of signaling pathways, and interact with their environment by qualitatively and quantitatively modifying their intracellular, surface, and extracellular proteomes. How this delicate communication takes place is a hot topic in cell biological research, and has important implications for human disease.

Prolonged Exposure to Social Stress Impairs Homeostatic Sleep Regulation

Stress and sleep are tightly regulated as a result of the substantial overlap in neurotransmitter signaling and regulatory pathways between the neural centers that modulate mood and sleep-wake cycle. The chronicity of the stressor and variability in coping with it are major determinants of the psychiatric outcomes and subsequent effect on sleep. The regulation of sleep is mediated by the interaction of a homeostatic and a circadian process according to the two-process model. Chronic stress induces stress-related disorders which are associated with deficient sleep homeostasis. However, little is known about how chronic stress affects sleep homeostasis and whether the differences in adaptation to stress distinctively influence sleep. Therefore, we assessed sleep homeostasis in C57BL6/J mice following exposure to 15-d of chronic social defeat stress. We implemented wake:sleep ratio as a behavioral correlate of sleep pressure. Both stress-resilient and stress-susceptible mice displayed deficient sleep homeostasis in post-stress baseline sleep. This was due to poor temporal correlation between frontal slow wave activity (SWA) power and sleep pressure in the dark/active phase. Moreover, the buildup rate of sleep pressure in the dark was lower in susceptible mice in comparison to stress-naïve mice. Additionally, 4-h SD in the dark caused a deficient sleep recovery response in susceptible mice characterized by non-rapid eye movement (NREM) sleep loss. Our findings provide evidence of deficient homeostatic sleep process (S) in baseline sleep in stress-exposed mice, while impaired sleep recovery following a mild enforced wakefulness experienced during the dark was only detected in stress-susceptible mice. This alludes to the differential homeostatic adaptation to stress between susceptible and resilient mice and its effect on sleep regulation.

Fine-tuned control of stress priming and thermotolerance

A common signature of cell adaptation to stress is the improved resistance upon priming by prior stress exposure. In the context of hyperthermia, priming or preconditioning with sublethal heat shock can be a useful tool to confer thermotolerance and competitive advantage to cells. In the present study, we develop a data-driven modeling framework that is simple and generic enough to capture a broad set of adaptation behaviors to heat stress at both molecular and cellular levels. The model recovers the main features of thermotolerance and clarifies the tradeoff principles which maximize the thermotolerance effect. It therefore provides an effective predictive tool to design preconditioning and fractionation hyperthermia protocols for therapeutic purpose.

Remodelling of Nucleus-Vacuole Junctions During Metabolic and Proteostatic Stress

Cellular adaptation to stress and metabolic cues requires a coordinated response of different intracellular compartments, separated by semipermeable membranes. One way to facilitate interorganellar communication is via membrane contact sites, physical bridges between opposing organellar membranes formed by an array of tethering machineries. These contact sites are highly dynamic and establish an interconnected organellar network able to quickly respond to external and internal stress by changing size, abundance and molecular architecture. Here, we discuss recent work on nucleus-vacuole junctions, connecting yeast vacuoles with the nucleus. Appearing as small, single foci in mitotic cells, these contacts expand into one enlarged patch upon nutrient exhaustion and entry into quiescence or can be shaped into multiple large foci essential to sustain viability upon proteostatic stress at the nuclear envelope. We highlight the remarkable plasticity and rapid remodelling of these contact sites upon metabolic or proteostatic stress and their emerging importance for cellular fitness.