scholarly journals Key Role of CRF in the Skin Stress Response System

2013 ◽  
Vol 34 (6) ◽  
pp. 827-884 ◽  
Author(s):  
Andrzej T. Slominski ◽  
Michal A. Zmijewski ◽  
Blazej Zbytek ◽  
Desmond J. Tobin ◽  
Theoharis C. Theoharides ◽  
...  
Keyword(s):  
Stress Response ◽  
Response System ◽  
Stress Response System

scholarly journals Explaining inconsistent results in cancer quality of life studies: the role of the stress–response system

2008 ◽  
Vol 17 (2) ◽  
pp. 174-181 ◽  
Author(s):  
Harry van de Wiel ◽  
Erwin Geerts ◽  
Josette Hoekstra-Weebers
Keyword(s):  
Quality Of Life ◽  
Stress Response ◽  
Response System ◽  
Stress Response System

scholarly journals The Rcs stress response system regulator GumB modulates Serratia marcescens induced inflammation and bacterial proliferation in a rabbit keratitis model and cytotoxicity in vitro

2021 ◽  
Author(s):  
Eric G. Romanowski ◽  
Nicholas A. Stella ◽  
John E. Romanowski ◽  
Kathleen A. Yates ◽  
Deepinder K. Dhaliwal ◽  
...  
Keyword(s):  
Stress Response ◽  
Serratia Marcescens ◽  
Corneal Epithelial Cell ◽  
Epithelial Cell Line ◽  
Wild Type ◽  
Response System ◽  
Stress Response System ◽  
Mutant Phenotypes

In this study, we tested the hypothesis that the conserved bacterial IgaA-family protein, GumB, mediates microbial pathogenesis associated with Serratia marcescens ocular infections through regulation of the Rcs stress response system. The role of the Rcs system and bacterial stress response systems for microbial keratitis is not known, and the role of IgaA proteins in mammalian pathogenesis models has only been tested with partial function allele variants of Salmonella . Here we observed that a Rcs-activated gumB mutant had a >50-fold reduction in proliferation compared to the wild type within rabbit corneas at 48 h, and demonstrated a notable reduction in inflammation based on inflammatory signs, including the absence of hypopyons, and proinflammatory markers measured at the RNA and protein levels. The gumB mutant phenotypes could be complemented by wild-type gumB on a plasmid. We observed that bacteria with inactivated of the Rcs stress response system induced high levels of ocular inflammation and restored corneal virulence to the gumB mutant. The high virulence of the Δ rcsB mutant was dependent upon the ShlA cytolysin transporter ShlB. Similar results were found testing the cytotoxic effects of WT and mutant bacteria on a human corneal epithelial cell line in vitro . Together, these data indicate that GumB regulates virulence factor production through the Rcs system and this overall stress response system is a key mediator of a bacterium’s ability to induce vision-threatening keratitis.

The oxidative stress response system

2004 ◽  
pp. 59-76 ◽  
Author(s):  
André Korsloot ◽  
Cornelis A.M. van Gestel ◽  
Nico M. van Straalen
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Response System ◽  
Stress Response System

The Evolutionary Life History Model of Externalizing Personality: Bridging Human and Animal Personality Science to Connect Ultimate and Proximate Mechanisms Underlying Aggressive Dominance, Hostility, and Impulsive Sensation Seeking

2017 ◽  
Vol 21 (4) ◽  
pp. 330-353 ◽  
Author(s):  
Michael P. Hengartner
Keyword(s):  
Life History ◽  
Stress Response ◽  
Sensation Seeking ◽  
Inclusive Fitness ◽  
Interpersonal Behavior ◽  
Life History Strategies ◽  
Proximate Mechanisms ◽  
Response System ◽  
Trade Offs ◽  
Stress Response System

The present work proposes an evolutionary model of externalizing personality that defines variation in this broad psychobiological phenotype resulting from genetic influences and a conditional adaptation to high-risk environments with high extrinsic morbidity-mortality. Due to shared selection pressure, externalizing personality is coadapted to fast life history strategies and maximizes inclusive fitness under adverse environmental conditions by governing the major trade-offs between reproductive versus somatic functions, current versus future reproduction, and mating versus parenting efforts. According to this model, externalizing personality is a regulatory device at the interface between the individual and its environment that is mediated by 2 overlapping psychobiological systems, that is, the attachment and the stress-response system. The attachment system coordinates interpersonal behavior and intimacy in close relationships and the stress-response system regulates the responsivity to environmental challenge and both physiological and behavioral reactions to stress. These proximate mechanisms allow for the integration of neuroendocrinological processes underlying interindividual differences in externalizing personality. Hereinafter I further discuss the model's major implications for personality psychology, psychiatry, and public health policy.

scholarly journals The Cpx Stress Response System Potentiates the Fitness and Virulence of Uropathogenic Escherichia coli

2013 ◽  
Vol 81 (5) ◽  
pp. 1450-1459 ◽  
Author(s):  
Irina Debnath ◽  
J. Paul Norton ◽  
Amelia E. Barber ◽  
Elizabeth M. Ott ◽  
Bijaya K. Dhakal ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Stress Response ◽  
Aminoglycoside Antibiotic ◽  
Deletion Mutants ◽  
Content Type ◽  
Response System ◽  
Stress Response System ◽  
Tract Infections ◽  
Auxiliary Factor

ABSTRACTStrains of uropathogenicEscherichia coli(UPEC) are the primary cause of urinary tract infections, representing one of the most widespread and successful groups of pathogens on the planet. To colonize and persist within the urinary tract, UPEC must be able to sense and respond appropriately to environmental stresses, many of which can compromise the bacterial envelope. The Cpx two-component envelope stress response system is comprised of the inner membrane histidine kinase CpxA, the cytosolic response regulator CpxR, and the periplasmic auxiliary factor CpxP. Here, by using deletion mutants along with mouse and zebrafish infection models, we show that the Cpx system is critical to the fitness and virulence of two reference UPEC strains, the cystitis isolate UTI89 and the urosepsis isolate CFT073. Specifically, deletion of thecpxRAoperon impaired the ability of UTI89 to colonize the murine bladder and greatly reduced the virulence of CFT073 during both systemic and localized infections within zebrafish embryos. These defects coincided with diminished host cell invasion by UTI89 and increased sensitivity of both strains to complement-mediated killing and the aminoglycoside antibiotic amikacin. Results obtained with thecpxPdeletion mutants were more complicated, indicating variable strain-dependent and niche-specific requirements for this well-conserved auxiliary factor.

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