Stress, inflammation, and eicosanoids: an emerging perspective

Umamaheswaran, Sujanitha; Dasari, Santosh K.; Yang, Peiying; Lutgendorf, Susan K.; Sood, Anil K.

doi:10.1007/s10555-018-9741-1

Cited by 50 publications

(49 citation statements)

References 109 publications

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“…Several studies implicate the role of lipids and lipid metabolism in inflammatory responses (Janciauskiene and Wright, 1998;Kang and Rivest, 2012;Zhang et al, 2018;Ntambi, 2019). Eicosanoids are a class of lipid mediators inflammation produced by innate immune cells that contribute to acute inflammation, resulting in pain, loss of function, heat, and swelling (Higgs et al, 1984;Williams and Higgs, 1988;Hedqvist et al, 1991;Umamaheswaran et al, 2018). Following the elimination of toxic stimuli, innate immune cells cease the production of eicosanoids and begin production of specialized pro-resolving lipid mediators (SPMs) to resolve inflammation (Serhan, 2010;Chandrasekharan and Sharma-Walia, 2015;Chiurchiu et al, 2018;Maclean et al, 2018).…”

Section: Lipids and Inflammationmentioning

confidence: 99%

Involvement of Lipids in Alzheimer’s Disease Pathology and Potential Therapies

2020

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Lipids constitute the bulk of the dry mass of the brain and have been associated with healthy function as well as the most common pathological conditions of the brain. Demographic factors, genetics, and lifestyles are the major factors that influence lipid metabolism and are also the key components of lipid disruption in Alzheimer's disease (AD). Additionally, the most common genetic risk factor of AD, APOE 4 genotype, is involved in lipid transport and metabolism. We propose that lipids are at the center of Alzheimer's disease pathology based on their involvement in the blood-brain barrier function, amyloid precursor protein (APP) processing, myelination, membrane remodeling, receptor signaling, inflammation, oxidation, and energy balance. Under healthy conditions, lipid homeostasis bestows a balanced cellular environment that enables the proper functioning of brain cells. However, under pathological conditions, dyshomeostasis of brain lipid composition can result in disturbed BBB, abnormal processing of APP, dysfunction in endocytosis/exocytosis/autophagocytosis, altered myelination, disturbed signaling, unbalanced energy metabolism, and enhanced inflammation. These lipid disturbances may contribute to abnormalities in brain function that are the hallmark of AD. The wide variance of lipid disturbances associated with brain function suggest that AD pathology may present as a complex interaction between several metabolic pathways that are augmented by risk factors such as age, genetics, and lifestyles. Herewith, we examine factors that influence brain lipid composition, review the association of lipids with all known facets of AD pathology, and offer pointers for potential therapies that target lipid pathways.

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Section: Lipids and Inflammationmentioning

confidence: 99%

Involvement of Lipids in Alzheimer’s Disease Pathology and Potential Therapies

2020

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“…Thus it was somewhat unexpected to see that FCS eicosanoid profiles were stable and clustered the FCS samples according to batches (Figure 2). This finding, supported by older and current literature reporting remarkable biological effects of eicosanoids 25,26,27 , motivated us to focus on this class of molecules. Functional analyses were to be based on spiking experiments with the U937 cells.…”

Section: Discussionmentioning

confidence: 74%

Eicosanoid content in fetal calf serum accounts for reproducibility challenges in cell culture

Niederstaetter¹,

Neuditschko

Brunmair³

et al. 2020

Preprint

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Reproducibility issues regarding in vitro cell culture experiments are related to genetic fluctuations and batch-wise variations of biological materials such as fetal calf serum (FCS). Genome sequencing may control the former, while the latter may remain unrecognized. Using a U937 macrophage model for cell differentiation and inflammation, we investigated whether the formation of effector molecules was dependent on the FCS batch used for cultivation. High resolution mass spectrometry was used to identify FCS constituents and to explore their effects on cultured cells evaluating secreted cytokines, eicosanoids and other inflammatory mediators. Remarkably, the FCS eicosanoid composition showed more batch-dependent variations than the protein composition. Efficient uptake of fatty acids from medium by U937 macrophages and inflammation-induced release thereof was evidenced using C13-labelled arachidonic acid, highlighting rapid lipid metabolism. For functional testing, FCS batch-dependent nanomolar concentration differences of two selected eicosanoids, 5-HETE and 15-HETE, were balanced out by spiking in. Culturing U937 cells at these defined conditions indeed resulted in significant proteome alterations indicating HETE-induced PPARγ activation, independently corroborated by HETE-induced formation of peroxisomes observed by high-resolution microscopy. In conclusion, the present data demonstrate that FCS-contained eicosanoids, subject to substantial batch-wise variation, may modulate cellular effector functions in cell culture experiments.

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“…Similarly, human athletes experienced a peak in plasma PGE 2 two hours after a two-hour high-intensity football training bout [12] and one hour after approximately 30 min of exhaustive treadmill running [25]. PGE 2 is a pro-inflammatory eicosanoid, reviewed in [26], which functions as a systemic pyrogen [27] and contributes to exercise-induced increases in core body temperature [28]. In the cardiac muscle, inducible PGE 2 (via Cox-2) plays an important role in late-phase ischemic preconditioning, which protects the heart from potentially catastrophic outcomes from ischemia [29].…”

Section: Discussionmentioning

confidence: 99%

The Time Course of Inflammatory Biomarkers Following a One-Hour Exercise Bout in Canines: A Pilot Study

Pearson

Pezzali

Donadelli

et al. 2020

Animals

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Simple Summary: The purpose of this study is to generate preliminary data on the inflammatory effects of an hour of hunting in dogs. Four basset hounds were set out to find a scent and freely adopted running or walking over wooded terrain for one hour. Blood samples were obtained before exercise and 1, 2, 4, 6, and 10 h after the end of the exercise for analysis of markers of inflammation (prostaglandin E 2 (PGE 2 ), nitric oxide (NO), interleukin 1β (IL-1β)), tumour necrosis factor-α (TNF-α)), and inflammation resolution (resolvin D1 (RvD1)). There was an increase in inflammation one hour after the exercise, shown by a significant increase in PGE 2 . Following the peak, PGE 2 steadily declined at the same time as RvD1 increased, with RvD1 peaking at six hours. This pilot study provides evidence that dogs that undergo an hour of hunt exercise experience transient inflammation that peaks one hour after the end of exercise; inflammation resolution peaks six hours after the end of exercise. Future studies should seek to further understand the distinct and combined roles of PGE 2 and RvD1 in dog adaptation to exercise stress.Abstract: There is little information available to describe the inflammatory consequences of and recovery from moderate-intensity exercise bouts in hunting dogs. The purpose of the current study is to generate pilot data on the appearance and disappearance of biomarkers of inflammation and inflammation resolution following a typical one-hour exercise bout in basset hounds. Four hounds were set out to find a scent and freely adopted running or walking over wooded terrain for approximately one hour. Venous blood samples were obtained before the exercise and at 1, 2, 4, 6, and 10 h following cessation of exercise and were analyzed for biomarkers of inflammation (prostaglandin E 2 (PGE 2 ), nitric oxide (NO), interleukin 1β (IL-1β)) tumour necrosis factor-α (TNF-α)), and inflammation resolution (resolvin D1 (RvD1)). There was an increase in inflammation one hour after the exercise, shown by a significant increase in PGE 2 . Following this peak, PGE 2 steadily declined at the same time as RvD1 increased, with RvD1 peaking at six hours. This pilot study provides evidence that dogs that undergo an hour of hunt exercise experience transient inflammation that peaks one hour after the end of exercise; inflammation resolution peaks six hours after the end of exercise. Future studies should seek to further understand the distinct and combined roles of PGE 2 and RvD1 in dog adaptation to exercise stress.

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Stress, inflammation, and eicosanoids: an emerging perspective

Cited by 50 publications

References 109 publications

Involvement of Lipids in Alzheimer’s Disease Pathology and Potential Therapies

Involvement of Lipids in Alzheimer’s Disease Pathology and Potential Therapies

Eicosanoid content in fetal calf serum accounts for reproducibility challenges in cell culture

The Time Course of Inflammatory Biomarkers Following a One-Hour Exercise Bout in Canines: A Pilot Study

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