// Huazhen Liu 1 , Yeshu Wang 2 , Qiaohuang Zeng 2 , Yu-Qun Zeng 2,3 , Chun-Ling Liang 1 , Feifei Qiu 1 , Hong Nie 4 and Zhenhua Dai 1 1 Section of Immunology, Guangdong Provincial Academy of Chinese Medical Sciences, and Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, Guangdong, P.R. China 2 Graduate School, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, P.R. China 3 Student Exchange Program, Mayo Clinic, Rochester, MN, USA 4 Guangdong Provincial Key Laboratory of Pharmacodynamic Constituents of TCM and New Drugs Research, College of Pharmacy, Jinan University, Guangzhou, Guangdong, P.R. China Correspondence to: Zhenhua Dai, email: // Keywords : transplantation, Treg, immunoregulation, T cell apoptosis, Immunology and Microbiology Section, Immune response, Immunity Received : January 21, 2017 Accepted : February 13, 2017 Published : February 20, 2017 Abstract Mounting evidence has shown that naturally occurring CD8+CD122+ T cells are regulatory T cells (Tregs) that suppress both autoimmunity and alloimmunity. We have previously shown that CD8+CD122+PD-1+ Tregs not only suppress allograft rejection, but also are more potent in suppression than conventional CD4+CD25+ Tregs. However, the mechanisms underlying their suppression of alloimmunity are not well understood. In an adoptive T-cell transfer model of mice lacking lymphocytes, we found that suppression of skin allograft rejection by CD8+CD122+PD-1+ Tregs was mostly dependent on their expression of Fas ligand as either lacking Fas ligand or blocking it with antibodies largely abolished their suppression of allograft rejection mediated by transferred T cells. Their suppression was also mostly reversed when effector T cells lacked Fas receptor. Indeed, these FasL+ Tregs induced T cell apoptosis in vitro in a Fas/FasL-dependent manner. However, their suppression of T cell proliferation in vitro was dependent on IL-10, but not FasL expression. Furthermore, adoptive transfer of CD8+CD122+PD-1+ Tregs significantly extended allograft survival even in wild-type mice if Tregs lacked Fas receptor or if recipients received recombinant IL-15, as these two measures synergistically expanded adoptively-transferred Tregs in recipients. Thus, this study may have important implications for Treg therapies in clinical transplantation.
Irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD) are inflammatory skin diseases accompanied by itch and pain. Irritant contact dermatitis is caused by chemical irritants eliciting an innate immune response, whereas ACD is induced by haptens additionally activating an adaptive immune response: After initial exposure (sensitization) to the hapten, a subsequent challenge can lead to a delayed-type hypersensitivity reaction. But, the sensory and inflammatory effects of sensitization (ICD) vs challenge of ACD are insufficiently studied. Therefore, we compared itch- and pain-like behaviors and inflammatory reactions evoked in mice during the sensitization (ICD) vs challenge phase (ACD) of application of the hapten, squaric acid dibutylester (SADBE).Our aim was to compare itch- and pain-like behaviors and inflammatory reactions evoked in mice during the sensitization (ICD) vs challenge phase (ACD) of application of the hapten, squaric acid dibutylester (SADBE).Mice were sensitized on the abdomen with 1% SADBE (ACD) or vehicle treated (ICD, control). Spontaneous and stimulus-evoked itch- and pain-like behaviors were recorded in mice before and after 3 daily challenges of the cheek with 1% SADBE (ACD, ICD). Cutaneous inflammation was evaluated with clinical scoring, ultrasound imaging, skin thickness, histology, and analyses of selected biomarkers for contact dermatitis, IL-1β, TNF-α, CXCL10, and CXCR3.Allergic contact dermatitis vs ICD mice exhibited more spontaneous site-directed scratching (itch) and wiping (pain). Allergic contact dermatitis-but not ICD-mice exhibited allodynia and hyperalgesia to mechanical and heat stimuli. Inflammatory mediators IL-1β and TNF-α were upregulated in both groups as well as the chemokine receptor, CXCR3. CXCL10, a CXCR3 ligand, was upregulated only for ACD. Inflammatory responses were more pronounced in ACD than ICD.These findings provide new information for differentiating the behavioral and inflammatory reactions to hapten-induced ICD and ACD.
Abstract Background: Galacto-oligosaccharides (GOS) is a commonly used as a prebiotic with a variety of metabolic benefits. Whether GOS plays a protective role in obesity is still unknown. Here we demonstrated that GOS possesses an anti-obesity activity by promoting adipose tissue browning and thermogenesis. Results: Our results showed that GOS effectively slow weight gain of diet-induced obese (DIO) rats without affecting energy intake. GOS significantly suppressed the hypertrophy and hyperplasia of white adipose tissue (WAT), as well as markedly lessened the ratio of fat pad to fat body. Consistently, GOS significantly improved serum total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) levels, which indicated an appropriate weight loss activity of GOS. Interestingly, GOS also significantly increased the expression levels of browning proteins (UCP1, PPARγ, PGC1α and PRMD16) both in the WAT and brown adipose tissue (BAT). We further found that GOS markedly increased the expression levels of LXRα, PPARα, LDLR and CYP7A1 proteins in the liver of obese rats. Conclusions: Taken together, we concluded that GOS inhibits obesity by accelerating the browning of white fat cells and the thermogenesis of brown fat cells, moreover GOS improves host lipid homeostasis by promoting cholesterol catabolism.
The aim of this study was to establish a method of isolating and culturing smooth muscle cells from the ductus deferens of rats. Smooth muscle cells were prepared from ductus deferens by explanting technique after dissection of adventitia and intimae, and cultured in vitro. The identification of the smooth muscle cells were verified by using anti α-smooth muscle actin (α-SMA) immunohistochemistry studies. The result suggested that the cells are multi-morphous, showing long fusiform or star shapes. The apophysis of cells contacted and coalesced to each other, in some regions the cells overlapped in multilayer, while in the other regions they formed monolayer that fluctuated and showed a peak-valley shape. They presented a positive reaction through immunohistochemistry studies. The purity of the cells was more than 99% through this method. The culturing of smooth muscle cells by explanting technique is simple and stable.
Abstract Pruritus is common in cholestatic liver disease, with a high clinical incidence rate and complex pathogenesis. Accumulation of potential pruritus inducers such as steroids, bile acids, and lysophosphatidic acid in the systemic circulation is the main cause of pruritus in cholestatic liver disease. Currently, clinical treatment of cholestatic liver disease-related pruritus mainly includes medication, intervention therapy, and some experimental methods. However, there are still problems, such as unclear pathological mechanisms and unsatisfactory treatment responses in some patients with cholestatic liver disease-related pruritus. Effective treatment for patients still faces challenges. By extensively screening patients' plasma (and/or bile) samples through clinical trials, potential pruritus inducers can be identified comprehensively, which can provide a deeper understanding of the itch signaling pathways in cholestatic liver disease and a basis for the development of treatment strategies. Traditional Chinese medicine (TCM) has shown certain characteristics and advantages in clinical treatment. Based on the etiology and pathogenesis, external application, internal administration, and TCM-specific therapies have achieved good clinical efficacy. Similarly, the combination of Chinese medicine and Western medicine has also achieved more effective treatment for patients with cholestatic liver disease-related pruritus. This article will introduce the latest progress in the study of pruritus inducers in cholestatic liver disease and its treatment in TCM and Western medicine.
To study the inhibitory effect of Luteolin on LPS-induced BV-2 cell.BV-2 cells were treated with LPS (0.1 microg/mL) for inflammation model; MTT assay was used to detect the viability of BV-2 cells; Nitric oxide (NO) was detected by the method of nitric acid reductase assay; Induce type II nitric oxide synthase (iNOS) enzyme activity was determined by type of nitric oxide synthase assay;TLR4 protein expression was examined by the Western Blot analysis.Luteolin significantly decreased the NO production and TLR4 protein expression as well as iNOS activity in LPS-activated microglial cell.LPS induced activation of microglia lead to inflammatory response and its mechanism may be related to inhibiting TLR4 signaling pathway.
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