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Stress Stimuli (stress + stimulus)
Selected AbstractsStress for maintaining memory: HSP70 as a mobile messenger for innate and adaptive immunityEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 6 2010Taoyong Chen Abstract HSP are abundant and conserved proteins present in all cells. Upon temperature shock or other stress stimuli, HSP are synthesized intracellularly, which may protect cells from protein denaturation or from death. Although HSP are synthesized intracellularly, HSP can also be mobilized to the plasma membrane or even be released under stress conditions. Elucidating the roles of cell surface and extracellular HSP in immune regulation has attracted much attention in recent years. Extracellularly, HSP can serve a cytokine function to initiate both innate and adaptive immunity through activation of APC. HSP serves also a chaperone function and facilitates presentation of antigen peptide to T cells. Similarly, cell surface HSP may activate APC and promote antigen presentation through cell,cell contact. A study in this issue of the European Journal of Immunology demonstrates that cell surface HSP70 on DC induced by stress can upregulate membrane-associated IL-15, which in turn promotes the proliferation of CD4+CD45RA memory T cells. Moreover, a DC-CD4+ T-cell interacting circuit formed by CD40L on T cells and CD40 on DC is proposed to play a role in the maintenance of memory homeostasis. This study has widened our view of HSP in adaptive immunity as well as their classical functions such as APC activator and antigen carrier. [source] Cross-talk involving extracellular sensors and extracellular alarmones gives early warning to unstressed Escherichia coli of impending lethal chemical stress and leads to induction of tolerance responsesJOURNAL OF APPLIED MICROBIOLOGY, Issue 5 2001R.J. Rowbury 1. Summary, 678 2. Introduction 2.1. Chemical and biological stress agents affecting enterobacteria, 678 2.2. Sensing of chemical and biological stress stimuli, 678 2.3. Intracellular sensors detect intracellularly-produced chemical stressing agents, 679 2.4. Intracellular sensors and intracellular induction components could delay response induction by extracellular chemical or biological stress agents, 680 2.5. Extracellular sensors and EICs give early warning of stress, 681 2.6. Disadvantages of extracellular components being needed for stress response induction, 682 2.7. Extracellular sensors and EICs allow stressed cells to warn unstressed ones, 682 2.8. A second role for some extracellular stress sensors, 683 3. Responses switched on by extracellular sensors and EICs 3.1. Involvement of EICs and ESCs in acid tolerance induction at pH 5·0 and at other mildly acidic pH values, 683 3.2. Further evidence for the obligate involvement of extracellular sensors and EICs in acid tolerance induction at pH 5·0, 684 3.3. On the nature of the acid pH tolerance-inducing ESC and EIC, 686 3.4. The acid tolerance ECs and their relation to other extracellular response-inducing components, 686 3.5. Extracellular components are needed for other inducible acid tolerance responses, 687 3.6. Involvement of EICs and extracellular sensors in acid tolerance in E. coli O157, 687 3.7. EICs involved in acid tolerance induction are diffusible, 687 4. Acid sensitization at alkaline pH and the role of extracellular sensor and EIC(s), 688 5. Responses affecting tolerance to alkali 5.1. Alkali sensitization at acidic pH, 688 5.2. Induced alkali tolerance at pH 9·0 and role of extracellular components, 688 6. Inducible tolerance to alkylhydroperoxides, 689 7. Are extracellular sensors and extracellular induction components needed for all stress responses?, 689 8. Altered responsiveness of extracellular sensors depending on growth conditions, 691 9. Protection of living cells from chemical stress by dead cultures, 691 10. How can intracellular levels of stress be detected?, 692 11. Are Nikolaev's extracellular ,protectants' and similar components related to EICs?, 693 12. Conclusions, 693 13. References, 694 [source] HSP70 interacts with TRAF2 and differentially regulates TNF, signalling in human colon cancer cellsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 3 2010Shengming Dai Abstract Members of tumour necrosis factor (TNF) family usually trigger both survival and apoptotic signals in various cell types. Heat shock proteins (HSPs) are conserved proteins implicated in protection of cells from stress stimuli. However, the mechanisms of HSPs in TNF,-induced signalling pathway have not been fully elucidated. We report here that HSP70 over-expression in human colon cancer cells can inhibit TNF,-induced NF,B activation but promote TNF,-induced activation of c-Jun N-terminal kinase (JNK) through interaction with TNF receptor (TNFR)-associated factor 2 (TRAF2). We provide evidence that HSP70 over-expression can sequester TRAF2 in detergent-soluble fractions possibly through interacting with TRAF2, leading to reduced recruitment of receptor-interacting protein (RIP1) and I,B, kinase (IKK) signalosome to the TNFR1,TRADD complex and inhibited NF,B activation after TNF, stimuli. In addition, we found that HSP70,TRAF2 interaction can promote TNF,-induced JNK activation. Therefore, our study suggests that HSP70 may differentially regulate TNF,-induced activation of NF,B and JNK through interaction with TRAF2, contributing to the pro-apoptotic roles of HSP70 in TNF,-induced apoptosis of human colon cancer cells. [source] Early signalling events in the Avr9/Cf-9-dependent plant defence responseMOLECULAR PLANT PATHOLOGY, Issue 1 2000Tina Romeis Resistance of tomato to the leaf mould fungus Cladosporium fulvum is controlled by the interaction between a plant-encoded resistance gene (Cf-9) and pathogen-encoded avirulence (Avr9) gene. Our objective is to understand the underlying molecular mechanisms that transmit the Cf-9/Avr9-dependent pathogen perception event and activate the plant defence response. Our approach toward the understanding of Cf -function is based on the analysis of early Cf-9/Avr9-mediated responses and signalling events. Because Cf-9 transgenically expressed in tobacco retains its specificity and activity to the Avr9 elicitor, signalling experiments were conducted in the heterologous system using these transgenic lines or derived Cf9 tobacco cell cultures. Among the earliest responses to the Avr9/Cf-9 elicitation event were rapid changes in ion-fluxes, the synthesis of active oxygen species (AOS), probably catalysed by a plant NADPH-oxidase, and the transient activation of two MAP kinases. These kinases were identified as WIPK (wounding-induced protein kinase) and SIPK (salicylic-acid induced kinase) from tobacco. Studies with pharmacological inhibitors suggested that the MAP kinases are located in an independent signalling pathway from the Avr9/Cf-9-dependent synthesis of AOS. SIPK and WIPK were involved in pathogen-related elicitation processes as well as in abiotic stress responses. This indicates that the plant defence is triggered via a signalling network that shares components with pathways originating from abiotic environmental stress stimuli. [source] Constitutive activation of MAPK cascade in acute quadriplegic myopathyANNALS OF NEUROLOGY, Issue 2 2004Simone Di Giovanni MD Acute quadriplegic myopathy (AQM; also called "critical illness myopathy") shows acute muscle wasting and weakness and is experienced by some patients with severe systemic illness, often associated with administration of corticosteroids and/or neuroblocking agents. Key aspects of AQM include muscle atrophy and myofilament loss. Although these features are shared with neurogenic atrophy, myogenic atrophy in AQM appears mechanistically distinct from neurogenic atrophy. Using muscle biopsies from AQM, neurogenic atrophy, and normal controls, we show that both myogenic and neurogenic atrophy share induction of myofiber-specific ubiquitin/proteosome pathways (eg, atrogin-1). However, AQM patient muscle showed a specific strong induction of transforming growth factor (TGF),,/MAPK pathways. Atrophic AQM myofibers showed coexpression of TGF-, receptors, p38 MAPK, c-jun, and c-myc, including phosphorylated active forms, and these same fibers showed apoptotic features. Our data suggest a model of AQM pathogenesis in which stress stimuli (sepsis, corticosteroids, pH imbalance, osmotic imbalance) converge on the TGF-, pathway in myofibers. The acute stimulation of the TGF-,/MAPK pathway, coupled with the inactivity-induced atrogin-1/proteosome pathway, leads to the acute muscle loss seen in AQM patients. Ann Neurol 2004 [source] Protein synthesis inhibition before or after stress exposure results in divergent endocrine and BDNF responses disassociated from behavioral responsesDEPRESSION AND ANXIETY, Issue 5 2008Nitsan Kozlovsky Ph.D. Abstract This study aimed to assess the effects of anisomycin, a protein synthesis inhibitor, on behavioral responses, brain-derived neurotrophic factor (BDNF) and TrkB mRNA levels, and circulating corticosterone in rats,when administered before or after initial exposure to a predator scent stress stimulus. Magnitude of changes in prevalence of anxiety-like behaviors on the elevated plus-maze and exaggerated startle reaction as well as corticosterone levels and mRNA BDNF and TrkB were compared in rats exposed to predator stress, microinjected with anisomycin before or after stress exposure. Administration of anisomycin before or after stress exposure reduced anxiety-like behavior in the elevated plus-maze and reduced the mean startle amplitude 7 days postexposure. Although the behavioral responses were similar when anisomycin was microinjected before or after stress exposure, the levels of mRNAs for BDNF and TrkB, which play a role in modulation of synaptic plasticity and the consolidation process, showed varying responses. Depression and Anxiety 0:1,11, 2007. © 2007 Wiley-Liss, Inc. [source] Regulation of the immune response by stress-activated protein kinasesIMMUNOLOGICAL REVIEWS, Issue 1 2009Mercedes Rincón Summary:, Activation of immune cells to mediate an immune response is often triggered by potential ,danger' or ,stress' stimuli that the organism receives. Within the mitogen-activated protein kinases (MAPKs) family, the stress-activated protein kinase (SAPK) group was defined as group of kinases that activated by stimuli that cause cell stress. In the immune cells, SAPKs are activated by antigen receptors (B- or T-cell receptors), Toll-like receptors, cytokine receptors, and physical,chemical changes in the environment among other stimuli. The SAPKs are established to be important mediators of intracellular signaling during adaptive and innate immune responses. Here we summarize what is currently known about the role of two sub-groups of SAPKs , c-Jun NH2 -terminal kinase and p38 MAPK-in the function of specific components of the immune system and the overall contribution to the immune response. [source] | |||||||||||||