Camel whey protein protects lymphocytes from apoptosis via the PI3K–AKT, NF-κB, ATF-3, and HSP-70 signaling pathways in heat-stressed male mice

2018 ◽  
Vol 96 (4) ◽  
pp. 407-416 ◽  
Author(s):  
Gamal Badr ◽  
Nancy K. Ramadan ◽  
Hanem S. Abdel-Tawab ◽  
Samia F. Ahmed ◽  
Mohamed H. Mahmoud
Keyword(s):  
Reactive Oxygen Species ◽  
B Cells ◽  
Whey Protein ◽  
Inflammatory Cytokines ◽  
Reactive Oxygen ◽  
Immune Dysfunction ◽  
Oxygen Species ◽  
Male Mice ◽  
The Impact ◽  
Pro Inflammatory Cytokines

Heat stress (HS) is an environmental factor that depresses the immune systems that mediate dysfunctional immune cells. Camel whey protein (CWP) can scavenge free radicals and enhance immunity. This study investigated the impact of dietary supplementation with CWP on immune dysfunction induced by exposure to HS. Male mice (n = 45) were distributed among 3 groups: control group; HS group; and HS mice that were orally administered CWP (HS + CWP group). The HS group exhibited elevated levels of reactive oxygen species (ROS) and pro-inflammatory cytokines (interleukin (IL)-1β, IL-6, tumor necrosis factor-α) as well as a significant reduction in the IL-2 and IL-4 levels. Exposure to HS resulted in impaired phosphorylation of AKT and IκB-α (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha); increased expression of activating transcription factor 3 (ATF-3) and 70 kDa heat shock proteins (HSP70); and aberrant distribution of CD3+ T cells and CD20+ B cells in the thymus and spleen. Interestingly, HS mice treated with CWP presented significantly restored levels of reactive oxygen species and pro-inflammatory cytokines near the levels observed in the control mice. Furthermore, supplementation of HS mice with CWP enhanced the phosphorylation of AKT and IκB-α; attenuated the expression of ATF-3, HSP70, and HSP90; and improved T and B cell distributions in the thymus and spleen. Our findings reveal a potential immunomodulatory effect of CWP in attenuating immune dysfunction induced by exposure to thermal stress.

scholarly journals Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells

2007 ◽  
Vol 85 (4) ◽  
pp. 462-472 ◽  
Author(s):  
Dongli Yang ◽  
Susan G. Elner ◽  
Zong-Mei Bian ◽  
Gerd O. Till ◽  
Howard R. Petty ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Inflammatory Cytokines ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Rpe Cells ◽  
Pro Inflammatory Cytokines

scholarly journals Action of chondroitin sulfate on the level of cytokines and reactive oxygen species in blood serum upon carrageenan-induced inflammation

2017 ◽  
Vol 22 (1) ◽  
pp. 9-11
Author(s):  
K. Dvorshchenko ◽  
M. Ashpin ◽  
O. Korotkyi ◽  
Ye. Torgalo ◽  
T. Falalyeyeva
Keyword(s):  
Reactive Oxygen Species ◽  
Blood Serum ◽  
Chondroitin Sulfate ◽  
Inflammatory Cytokines ◽  
Superoxide Radical ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tnf Α ◽  
Rat Paw ◽  
Pro Inflammatory Cytokines

Increase of concentration of pro-inflammatory cytokines (IL-1β, TNF-α) is fixed in blood serum at carrageenan-induced rat paw inflammation, as well as increase of the content of reactive oxygen species (superoxide radical, hydrogen peroxide). At introduction of the preparation on the basis of chondroitin sulfate the level of pro-inflammatory cytokines and reactive oxygen species in blood serum decreases, while the concentration of IL10 increases in 1,7 times concerning the group of animals with сarrageenan-induced inflammation.

scholarly journals Human Huntington’s disease pluripotent stem cell-derived microglia develop normally but are abnormally hyper-reactive and release elevated levels of reactive oxygen species

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Grace C. O’Regan ◽  
Sahar H. Farag ◽  
Caroline S. Casey ◽  
Alison Wood-Kaczmar ◽  
Jennifer M. Pocock ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Inflammatory Cytokines ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Protein Markers ◽  
Striatal Neurons ◽  
Human Microglia ◽  
Pro Inflammatory Cytokines

Abstract Background Neuroinflammation may contribute to the pathogenesis of Huntington’s disease, given evidence of activated microglia and elevated levels of inflammatory molecules in disease gene carriers, even those many years from symptom onset. We have shown previously that monocytes from Huntington’s disease patients are hyper-reactive to stimulation in a manner dependent on their autonomous expression of the disease-causing mutant HTT protein. To date, however, whether human microglia are similarly hyper-responsive in a cell-autonomous manner has not been determined. Methods Microglial-like cells were derived from human pluripotent stem cells (PSCs) expressing mutant HTT containing varying polyglutamine lengths. These included lines that are otherwise isogenic, such that any observed differences can be attributed with certainty to the disease mutation itself. Analyses by quantitative PCR and immunofluorescence microscopy respectively of key genes and protein markers were undertaken to determine whether Huntington’s disease PSCs differentiated normally to a microglial fate. The resultant cultures and their supernatants were then assessed by various biochemical assays and multiplex ELISAs for viability and responses to stimulation, including the release of pro-inflammatory cytokines and reactive oxygen species. Conditioned media were applied to PSC-derived striatal neurons, and vice versa, to determine the effects that the secretomes of each cell type might have on the other. Results Human PSCs generated microglia successfully irrespective of the expression of mutant HTT. These cells, however, were hyper-reactive to stimulation in the production of pro-inflammatory cytokines such as IL-6 and TNFα. They also released elevated levels of reactive oxygen species that have neurotoxic potential. Accompanying such phenotypes, human Huntington’s disease PSC-derived microglia showed increased levels of apoptosis and were more susceptible to exogenous stress. Such stress appeared to be induced by supernatants from human PSC-derived striatal neurons expressing mutant HTT with a long polyglutamine tract. Conclusions These studies show, for the first time, that human Huntington’s disease PSC-derived microglia are hyper-reactive due to their autonomous expression of mutant HTT. This provides a cellular basis for the contribution that neuroinflammation might make to Huntington’s disease pathogenesis.

scholarly journals Assessment of Physico-Chemical and Toxicological Properties of Commercial 2D Boron Nitride Nanopowder and Nanoplatelets

2021 ◽  
Vol 22 (2) ◽  
pp. 567
Author(s):  
Brixhilda Domi ◽  
Kapil Bhorkar ◽  
Carlos Rumbo ◽  
Labrini Sygellou ◽  
Spyros N. Yannopoulos ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Boron Nitride ◽  
A549 Cells ◽  
Reactive Oxygen ◽  
Slight Reduction ◽  
Oxygen Species ◽  
Potential Toxicity ◽  
Cellular Models ◽  
Physico Chemical ◽  
The Impact

Boron nitride (BN) nanomaterials have been increasingly explored for potential applications in chemistry and biology fields (e.g., biomedical, pharmaceutical, and energy industries) due to their unique physico-chemical properties. However, their safe utilization requires a profound knowledge on their potential toxicological and environmental impact. To date, BN nanoparticles have been considered to have a high biocompatibility degree, but in some cases, contradictory results on their potential toxicity have been reported. Therefore, in the present study, we assessed two commercial 2D BN samples, namely BN-nanopowder (BN-PW) and BN-nanoplatelet (BN-PL), with the objective to identify whether distinct physico-chemical features may have an influence on the biological responses of exposed cellular models. Morphological, structural, and composition analyses showed that the most remarkable difference between both commercial samples was the diameter of their disk-like shape, which was of 200–300 nm for BN-PL and 100–150 nm for BN-PW. Their potential toxicity was investigated using adenocarcinomic human alveolar basal epithelial cells (A549 cells) and the unicellular fungus Saccharomycescerevisiae, as human and environmental eukaryotic models respectively, employing in vitro assays. In both cases, cellular viability assays and reactive oxygen species (ROS) determinations where performed. The impact of the selected nanomaterials in the viability of both unicellular models was very low, with only a slight reduction of S. cerevisiae colony forming units being observed after a long exposure period (24 h) to high concentrations (800 mg/L) of both nanomaterials. Similarly, BN-PW and BN-PL showed a low capacity to induce the formation of reactive oxygen species in the studied conditions. Even at the highest concentration and exposure times, no major cytotoxicity indicators were observed in human cells and yeast. The results obtained in the present study provide novel insights into the safety of 2D BN nanomaterials, indicating no significant differences in the toxicological potential of similar commercial products with a distinct lateral size, which showed to be safe products in the concentrations and exposure conditions tested.

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