1.
Chronic Stress Contributes to Osteosarcopenic Adiposity via Inflammation and Immune Modulation: The Case for More Precise Nutritional Investigation.
Ilich, JZ, Gilman, JC, Cvijetic, S, Boschiero, D
Nutrients. 2020;(4)
Abstract
Chronic stress and low-grade chronic inflammation (LGCI) are key underlying factors formany diseases, including bone and body composition impairments. Objectives of this narrativereview were to examine the mechanisms by which chronic stress and LGCI may influenceosteosarcopenic adiposity (OSA) syndrome, originally named as ostoesarcopenic obesity (OSO).We also examined the crucial nutrients presumed to be affected by or cause of stress andinflammation and compared/contrasted them to those of our prehistoric ancestors. The evidenceshows that stress (particularly chronic) and its related inflammatory processes, contribute toosteoporosis, sarcopenia, and adiposity ultimately leading to OSA as a final and most derangedstate of body composition, commencing at the mesenchymal cell lineage disturbance. Thefoods/nutrients consumed by modern humans, as well as their altered lifestyle, also contribute tostress, LGCI and subsequently to OSA. The processes can also go in opposite direction when stressand inflammation impact nutritional status, particularly some micronutrients' levels. Whilenutritional management of body composition and LGCI have been studied, the nutrients (and theirquantities) most affected by stressors and those which may act toward the alleviation of stressfulstate, ultimately leading to better body composition outcomes, need to be elucidated.
2.
The impact of sport related stressors on immunity and illness risk in team-sport athletes.
Keaney, LC, Kilding, AE, Merien, F, Dulson, DK
Journal of science and medicine in sport. 2018;(12):1192-1199
Abstract
OBJECTIVES Elite team-sport athletes are frequently exposed to stressors that have the potential to depress immunity and increase infection risk. Therefore, the purpose of this review is to describe how team-sport stressors impact upon immune responses, along with exploring whether alterations in these markers have the potential to predict upper respiratory tract illness symptoms. DESIGN Narrative review. METHODS Salivary secretory immunoglobulin A (SIgA) and T-cell markers have been shown to predict infection risk in individual endurance athletes. Papers discussing the impact of team-sport stressors on SIgA and T-cells were discussed in the review, studies discussing other aspects of immunity were excluded. Journal articles were sourced from PubMed, Web of science and Scopus. Key search terms included team-sport athletes, stressors, immunity, T-cells, cytokines, SIgA and upper respiratory illness. RESULTS Most team-sport stressors appear to increase risk for illness. An association between reduced SIgA and increased illness incidence has been demonstrated. Intensive training and competition periods have been shown to reduce SIgA, however, it is less clear how additional stressors including extreme environmental conditions, travel, psychological stress, sleep disturbance and poor nutrition affect immune responses. CONCLUSIONS Monitoring SIgA may provide an assessment of a team-sport athletes risk status for developing upper respiratory tract symptoms, however there is currently not enough evidence to suggest SIgA alone can predict illness. Team-sport stressors challenge immunity and it is possible that the combination of stressors could have a compounding effect on immunodepression and infection risk. Given that illness can disrupt training and performance, further research is required to better elucidate how stressors individually and collectively influence immunity and illness.
3.
The Transcription Factor EB Links Cellular Stress to the Immune Response
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Nabar, NR, Kehrl, JH
The Yale journal of biology and medicine. 2017;(2):301-315
Abstract
The transcription factor EB (TFEB) is the master transcriptional regulator of autophagy and lysosome biogenesis. Recent advances have led to a paradigm shift in our understanding of lysosomes from a housekeeping cellular waste bin to a dynamically regulated pathway that is efficiently turned up or down based on cellular needs. TFEB coordinates the cellular response to nutrient deprivation and other forms of cell stress through the lysosome system, and regulates a myriad of cellular processes associated with this system including endocytosis, phagocytosis, autophagy, and lysosomal exocytosis. Autophagy and the endolysosomal system are critical to both the innate and adaptive arms of the immune system, with functions in effector cell priming and direct pathogen clearance. Recent studies have linked TFEB to the regulation of the immune response through the endolysosmal pathway and by direct transcriptional activation of immune related genes. In this review, we discuss the current understanding of TFEB's function and the molecular mechanisms behind TFEB activation. Finally, we discuss recent advances linking TFEB to the immune response that positions lysosomal signaling as a potential target for immune modulation.