17 research outputs found
Ion channels enable electrical communication in bacterial communities
The study of bacterial ion channels has provided fundamental insights into the structural basis of neuronal signalling; however, the native role of ion channels in bacteria has remained elusive. Here we show that ion channels conduct long-range electrical signals within bacterial biofilm communities through spatially propagating waves of potassium. These waves result from a positive feedback loop, in which a metabolic trigger induces release of intracellular potassium, which in turn depolarizes neighbouring cells. Propagating through the biofilm, this wave of depolarization coordinates metabolic states among cells in the interior and periphery of the biofilm. Deletion of the potassium channel abolishes this response. As predicted by a mathematical model, we further show that spatial propagation can be hindered by specific genetic perturbations to potassium channel gating. Together, these results demonstrate a function for ion channels in bacterial biofilms, and provide a prokaryotic paradigm for active, long-range electrical signalling in cellular communities.J.G.-O. is supported by the Ministerio de Economia y Competitividad (Spain) and FEDER, under project FIS2012-37655-C02-01, and by the ICREA Academia Programme. This research was funded by the National Institutes of Health, National Institute of General Medical Sciences Grant R01 GM088428 and the National Science Foundation Grant MCB-1450867 50867 (both to G.M.S.). This work was also supported by the San Diego Center for Systems Biology (NIH Grant P50 GM085764
Physical activity, job demand–control, perceived stress–energy, and salivary cortisol in white-collar workers
Genetically encoded fluorescent indicators for imaging intracellular potassium ion concentration
Leishmania RNA virus exacerbates Leishmaniasis by subverting innate immunity via TLR3-mediated NLRP3 inflammasome inhibition
Does physical activity reduce risk for Alzheimer’s disease through interaction with the stress neuroendocrine system?
Lack of physical activity (PA) is a risk factor for Alzheimer's disease (AD) and PA interventions are believed to provide an effective non-pharmacological approach for attenuating the symptoms of this disease. However, the mechanism of action of these positive effects is currently unknown. It is possible that the benefits may be at least partially mediated by effects on the neuroendocrine stress system. Chronic stress can lead to dysfunction of the hypothalamic pituitary adrenal (HPA) axis, leading to aberrant basal and circadian patterns of cortisol secretion and a cascade of negative downstream events. These factors have been linked not only to reduced cognitive function in the non-demented but also increased levels of Amyloid β plaques and protein Tau "tangles" (the neuropathological hallmarks of AD) in mouse models of this disease. However, there is evidence that PA can have restorative effects on the stress neuroendocrine system and related risk factors relevant to AD. We explore the possibility that PA can positively impact upon AD by restoring normative HPA axis function, with consequent downstream effects upon underlying neuropathology and associated cognitive function. We conclude with suggestions for future research to test this hypothesis in patients with AD
Mechanisms and treatment of organ failure in sepsis.
Sepsis is a dysregulated immune response to an infection that leads to organ dysfunction. Knowledge of the pathophysiology of organ failure in sepsis is crucial for optimizing the management and treatment of patients and for the development of potential new therapies. In clinical practice, six major organ systems - the cardiovascular (including the microcirculation), respiratory, renal, neurological, haematological and hepatic systems - can be assessed and monitored, whereas others, such as the gut, are less accessible. Over the past 2 decades, considerable amounts of new data have helped improve our understanding of sepsis pathophysiology, including the regulation of inflammatory pathways and the role played by immune suppression during sepsis. The effects of impaired cellular function, including mitochondrial dysfunction and altered cell death mechanisms, on the development of organ dysfunction are also being unravelled. Insights have been gained into interactions between key organs (such as the kidneys and the gut) and organ-organ crosstalk during sepsis. The important role of the microcirculation in sepsis is increasingly apparent, and new techniques have been developed that make it possible to visualize the microcirculation at the bedside, although these techniques are only research tools at present.SCOPUS: re.jinfo:eu-repo/semantics/publishe