This study investigated the effect of fermentation on the physicochemical properties of b-glucans in oat sourdough. Sourdoughs were produced from oat using homo-fermentative lactic acid bacteria, Lactobacillus plantarum 22134. The contents of total b-glucan and soluble b-glucan, the molecular weight (MW) of b-glucan and the viscosity of the extracted b-glucans were determined at 0, 4, 8, 10 and 12 h of fermentation. The total b-glucan content decreased from 4.89% to 4.23% after 12 h of fermentation. The soluble b-glucan concentration increased from 1.89% to 2.18% and then decreased to 1.97% after 8 h of fermentation. The content of b-glucans with MW > 10 5 decreased from 0 to 4 h of fermentation, followed by an increase and then a decrease after 8 h. The oat sourdough fermented for 8 h had high viscosity, which could be more beneficial for health and bread texture quality, especially for gluten-free breads.
Background and AimsWheat gluten is a critical trigger for celiac disease, often causing inflammatory lesions and oxidative stress damage in the intestines of patients. In daily life, it is difficult for celiac disease patients to strictly avoid the dietary intake of gluten, which makes complementary preventive therapy particularly urgent. As such, we investigated the alleviating effects of resveratrol in vivo and in vitro models of celiac disease.MethodsWe established in vivo and in vitro models of gluten protein-induced celiac disease. The intervention effect of resveratrol was defined well based on relevant indicators of inflammation, immunity and oxidative stress, and its possible involvement in signaling pathways and genes were also identified.ResultsResveratrol was effective in reducing intestinal oxidative stress and inflammatory damage induced by wheat gluten in both cell and mouse models for celiac disease. We identified correlations between the genes (Fgf15, Nr0b2, Aire and Ubd) and signaling pathways (PPAR, AMPK and FoxO) in which resveratrol performed critical roles.ConclusionsResveratrol contributed to regulate development of autoimmunity through up-regulation of Aire and Ubd genes and promote nutrient absorption in intestine through down-regulation of Fgf15 and Nr0b2 genes, as well as played a role in regulating complex response system of oxidative stress, inflammatory response and immune response in intestine by activating PPAR, AMPK and FoxO signaling pathways, thus effectively alleviating the intestinal symptoms of celiac disease.
CD8+ T cells are the key executioners of the adaptive immune arm, which mediates antitumor and antiviral immunity. Naïve CD8+ T cells develop in the thymus and are quickly activated in the periphery after encountering a cognate antigen, which induces these cells to proliferate and differentiate into effector cells that fight the initial infection. Simultaneously, a fraction of these cells become long-lived memory CD8+ T cells that combat future infections. Notably, the generation and maintenance of memory cells is profoundly affected by various in vivo conditions, such as the mode of primary activation (e.g., acute vs. chronic immunization) or fluctuations in host metabolic, inflammatory, or aging factors. Therefore, many T cells may be lost or become exhausted and no longer functional. Complicated intracellular signaling pathways, transcription factors, epigenetic modifications, and metabolic processes are involved in this process. Therefore, understanding the cellular and molecular basis for the generation and fate of memory and exhausted CD8+ cells is central for harnessing cellular immunity. In this review, we focus on mammalian target of rapamycin (mTOR), particularly signaling mediated by mTOR complex (mTORC) 2 in memory and exhausted CD8+ T cells at the molecular level.
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