ARCHIVES OF DERMATOLOGICAL RESEARCH
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2025
·Vol. 317
·期 1
·1-16
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IF 2.1
Lin Ling,Li Wei,Gao Xinjing,Li Qian,Zhou Xin,Liu Weiyu,Zhong Xuelian,Yang Yunqing,Zhang Xibao,Luo Quan
Psoriasis represents a chronic inflammatory skin disease occurring globally. We investigated the role of plasma exosomal microRNA (miR)- 148a- 3p and its target gene Bim in psoriasis. Plasma exosomes (Exos) and CD4 + T cells were extracted from psoriatic patients. miR- 148a- 3p expression in Exos and CD4 + T cells of psoriatic patients, the proportions of CD4 + T cell subsets, and the contents of anti-inflammatory/pro-inflammatory factors were determined by RT-qPCR, flow cytometry and ELISA. The correlation between plasma exosomal miR- 148a- 3p and CD4 + T cell subsets in psoriatic patients was analyzed by Pearson’s analysis. The psoriatic mouse was treated with Exos/antagomir miR- 148a- 3p. Histopathological changes in the skin were observed. The CD4 + T cell subset levels, serum cytokine contents and miR- 148a- 3p expression in the blood were measured. The miR- 148a- 3p-Bim targeted binding relationship was predicted and verified by Starbase database and dual-luciferase assay. The Bim expression in psoriatic mice was determined. Psoriatic patients had highly-expressed miR- 148a- 3p in both Exos and CD4 + T cells, and abnormal CD4 + T cell subsets and cytokine levels. Plasma exosomal miR- 148a- 3p was correlated with the CD4 + T cell subsets in psoriatic patients. Exos caused down-regulated miR- 148a- 3p level in skin tissues of mouse, regulated CD4 + T cell function and aggravated the symptoms in psoriatic mice. miR- 148a- 3p repression partially reversed the role of Exos in CD4 + T cell function and psoriasis-like symptoms. Exos-carried miR- 148a- 3p targeted Bim in CD4 + T cells of psoriatic mice. Plasma exosomal miR- 148a- 3p targeted Bim to affect the dysfunction of CD4 + T cells in psoriatic mice, thereby aggravating the psoriasis-like symptoms.
研究领域:
皮肤病学
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分子生物学
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免疫学
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DOI
PubMed
高影响因子
Clinical and Vaccine Immunology
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2005
·Vol. 12
·期 11
·
IF 0
Yongjun Jiang,Hong Shang,Zining Zhang,Yingying Diao,Di Dai,Wenqing Geng,Min Zhang,Xiaoxu Han,Yanan Wang,Jing Liu
Natural killer (NK) cells, natural killer T (NKT) cells, and T lymphocytes were analyzed by using a flow cytometer in 225 human immunodeficiency virus (HIV)-positive individuals infected through the past sale of blood and plasma without receiving antiretroviral therapy in the People’s Republic of China. According to CD4 T-cell counts these HIV-infected adults were stratified into three groups: long-term slow progressors, HIV-infected subjects, and AIDS patients. NK cell counts in long-term slow progressors were higher compared to HIV infection and AIDS patients (P < 0.05) and lower compared to normal controls (P < 0.05), whereas NKT cell counts in slow progressors and the HIV infection group were not different from those of normal controls. NK cell counts in HIV-seropositive subjects were positively correlated with CD4 T-cell counts (P < 0.05), and NKT cell counts were positively correlated with CD4 T-cell and CD8 T-cell counts (P < 0.05). The CD8 T-cell counts were higher in slow progressors compared to those with HIV infection, AIDS patients, and normal controls. These results indicated that HIV infection causes alterations of NK cells and T cells in slow progressors, HIV-infected subjects, and AIDS patient groups, but no difference was found in NKT cell counts and percentages in slow progressors and the HIV-infected group compared to normal controls.
研究领域:
免疫学
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病毒学
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DOI
PubMed
MOLECULAR IMMUNOLOGY
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2023
·
IF 3.6
Wei Zhong,Leheng Feng,Wei Tian,Hongbo Qu,Haibo Xu,Ke Ning,Li Liu,Wei Liu,Xiaowei Gong,Hong Chen
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease . This study aimed to investigate the role of SMAD specific E3 ubiquitin protein ligase 1 (SMURF1) in the Th17 and Th17.1 differentiation and Treg/Th17 imbalance, which are major factors contributing to the pathogenesis of SLE. SLE patients and healthy individuals were recruited to detect the SMURF1 levels in naïve CD4 + cells from peripheral blood. Purified and expanded naïve CD4 + T cells were employed to evaluate the effects of SMURF1 on Th17 and Th17.1 polarization in vitro. MRL/lpr lupus model was employed to explore the disease phenotype as well as Treg/Th17 balance in vivo. The results showed that SMURF1 was down-regulated in naïve CD4 + T cells in peripheral blood of patients with SLE and in spleen of MRL/lpr mice. SMURF1 overexpression suppressed the polarization of naïve CD4 + T cells toward Th17 and Th17.1 phenotype and down-regulated the expression of retinoid-related orphan receptor-gammat (RORγt). Subsequently, SMURF1 down-regulation aggravated the disease phenotype, inflammation, and the Treg/Th17 imbalance in MRL/lpr mice. Furthermore, we found that SMURF overexpression promoted the ubiquitination and decreases the stability of RORγt. In conclusion, SMURF1 inhibited the polarization of Th17 and Th17.1 cells and improved the Treg/Th17 imbalance in SLE, which was mediated as least partly by the ubiquitination of RORγt.
研究领域:
免疫学
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自身免疫性疾病
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
Food & Function
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2025
·
IF 5.4
Junzhu Li,Xin Feng,Yizhi Jing,Haidong Qian,Yun Ji,Yanling Hao,Zhengyuan Zhai
Infectious enteritis is a chronic inflammatory condition of the intestine, mainly characterized by immune cell infiltration and gut microbiota dysbiosis. Resveratrol, a natural polyphenol compound from grapes, berries and peanuts, is known for its antioxidant and anti-inflammatory properties. This study investigated the effects of resveratrol in a murine model of Citrobacter rodentium-induced colitis. Resveratrol ameliorated disease symptoms, body weight loss, colon shortening, and increased intestinal permeability. Histological and immunofluorescence analyses revealed that resveratrol improved intestinal barrier integrity by increasing goblet cells, upregulating MUC-2 expression, reducing crypt hyperplasia, and suppressing epithelial cell apoptosis. Resveratrol significantly decreased the mRNA levels of pro-inflammatory cytokines, namely Tumor Necrosis Factor-α (TNF-α), Interleukin-6 (IL-6) and Interleukin-22 (IL-22), while restoring the percentage of CD4+ cells to normal levels. It also attenuated oxidative stress by enhancing the activities of key antioxidant enzymes, including catalase (CAT), total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px). Furthermore, resveratrol reshaped the gut microbiota by increasing the abundance of obligate anaerobes Clostridium and decreasing the abundance of facultative anaerobes Enterobacteriaceae. The abundance of Lactobacillus and Dubosiella was also significantly increased by resveratrol. In summary, these findings demonstrate that resveratrol supplementation may serve as a promising nutritional strategy to ameliorate C. rodentium colitis by inhibiting CD4+ cell activation and remodeling the gut microbiota.
研究领域:
微生物组学
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免疫学
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炎症性肠病
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营养免疫
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分子营养学
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肠道屏障功能
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产品关联
DOI
PubMed
高影响因子
Frontiers in Neuroscience
·
2022
·
IF 5.152
Yan-Lin Chen,Lan Bai,Dilirebati Dilimulati,Shuai Shao,Che Qiu,Ting Liu,Shuo Xu,Xue-Bing Bai,Lin-Juan Du,Lu-Jun Zhou,Wen-Zhen Lin,Xiao-Qian Meng,Yi-Chao Jin,Yan Liu,Xiao-Hua Zhang,Sheng-Zhong Duan,Feng Jia
Although epidemiological studies suggest that periodontitis is tightly associated with ischemic stroke, its impact on ischemic stroke and the underlysing mechanisms are poorly understood. Recent studies have shown that alteration in gut microbiota composition influences the outcomes of ischemic stroke. In the state of periodontitis, many oral pathogenic bacteria in the saliva are swallowed and transmitted to the gut. However, the role of periodontitis microbiota in the pathogenesis and progression of ischemic stroke is unclear. Therefore, we hypothesized that the periodontitis salivary microbiota influences the gut immune system and aggravates ischemic stroke. Mice receiving gavage of periodontitis salivary microbiota showed significantly worse stroke outcomes. And these mice also manifested more severe neuroinflammation, with higher infiltration of inflammatory cells and expression of inflammatory cytokines in the ischemic brain. More accumulation of Th17 cells and IL-17 + γδ T cells were observed in the ileum. And in Kaede transgenic mice after photoconversion. Migration of CD4 + T cells and γδ T cells from the ileum to the brain was observed after ischemic stroke in photoconverted Kaede transgenic mice. Furthermore, the worse stroke outcome was abolished in the IL-17A knockout mice. These findings suggest that periodontitis salivary microbiota increased IL-17A-producing immune cells in the gut, likely promoted the migration of these cells from the gut to the brain, and subsequently provoked neuroinflammation after ischemic stroke. These findings have revealed the role of periodontitis in ischemic stroke through the gut and provided new insights into the worse outcome of ischemic stroke coexisting with periodontitis in clinical trials.
研究领域:
神经科学
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免疫学
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微生物学
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病理学
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产品关联
DOI
PubMed
高影响因子
Small
·
2024
·
IF 13
Jiabao Dong,Xupeng Chai,Yucheng Xue,Shiyun Shen,Zhuo Chen,Zetao Wang,Eloy Yinwang,Shengdong Wang,Liang Chen,Fengfeng Wu,Hengyuan Li,Zehao Chen,Jianbin Xu,Zhaoming Ye,Xiongfeng Li,Qian Lu
Adoptive cellular therapy is a promising strategy for cancer treatment. However, the effectiveness of this therapy is limited by its intricate and immunosuppressive tumor microenvironment. In this study, a targeted therapeutic strategy for macrophage loading of drugs is presented to enhance anti-tumor efficacy of macrophages. K7M2-target peptide (KTP) is used to modify macrophages to enhance their affinity for tumors. Pexidartinib-loaded ZIF-8 nanoparticles (P@ZIF-8) are loaded into macrophages to synergistically alleviate the immunosuppressive tumor microenvironment synergistically. Thus, the M1 macrophages decorated with KTP carried P@ZIF-8 and are named P@ZIF/M1-KTP. The tumor volumes in the P@ZIF/M1-KTP group are significantly smaller than those in the other groups, indicating that P@ZIF/M1-KTP exhibited enhanced anti-tumor efficacy. Mechanistically, an increased ratio of CD4+ T cells and a decreased ratio of MDSCs in the tumor tissues after treatment with P@ZIF/M1-KTP indicated that it can alleviate the immunosuppressive tumor microenvironment. RNA-seq further confirms the enhanced immune cell function. Consequently, P@ZIF/M1-KTP has great potential as a novel adoptive cellular therapeutic strategy for tumors.
研究领域:
癌症生物学
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药学
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免疫治疗
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产品关联
DOI
PubMed
高影响因子
ACS Omega
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2022
·
IF 4.132
Yanju Gao,Bo Zhou,Han Zhang,Lin Chen,Xiaohong Wang,Hongbing Chen,Lin Zhou
Background: Ulcerative colitis (UC) is a chronic disease of the intestinal tract in which excessive activation of inflammatory response is correlated. l-Ergothioneine (EGT) widely existing in mushrooms has various physiological activities. In this study, the protective effects of EGT on dextran sulfate sodium (DSS)-induced colitis mice were investigated. Results: It was observed that EGT administration, especially at the high dose level, prevented the body weight loss, the colon shortening, and the increase in disease activity index and spleen index caused by DSS. Moreover, EGT supplementation attenuated DSS-induced gut barrier damage by enhancing the expression of tight-junction protein and recovering the loss of gut mucus layer. Furthermore, EGT considerably decreased the colonic myeloperoxidase (MPO) activity induced by DSS, but no significant differences were observed in the concentrations of IL-6 and TNF-α in colon tissues. Additionally, EGT downregulated the populations of CD4+ T cells and macrophages, indicating that EGT stabilized the immune response caused by DSS. Conclusion: Together these results suggest that EGT can alleviate DSS-induced colitis and provide important insights concerning the potential anticolitis activity of such food products.
研究领域:
免疫学
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胃肠病学
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药理学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2024
·
IF 7.7
Lele Gong,Yuanyuan Zhang,Lele Wang,Xuyang Zhao,Lucai Wang,Xiangqi Qiu,Xilong Yang,Wenhui Zhu,Lijie Lv,Yunzhe Kang,Yanan Wu,Angke Zhang,Yongkun Du,Xuannian Wang,Gaiping Zhang,Aijun Sun,Guoqing Zhuang
The African swine fever virus (ASFV) continues to pose significant economic and pandemic risks. Consequently, discovering new, efficient vaccines is crucial. Messenger RNA (mRNA) vaccines have emerged as promising candidates, providing minimal risk of insertional mutagenesis, high safety profiles, effectiveness, rapid scalability in production, and cost-effectiveness. In this study, we have developed an ASF p30 mRNA vaccine candidate (mRNA/Man-LNP) employing mannose-modified lipid nanoparticles (LNPs). The mRNA/Man-LNP exhibited effective antigen presentation and facilitated dendritic cells (DCs) maturation. Notably, it elicited strong IgG titers and activated CD4 + and CD8 + T-cells in immunized mice, all while adhering to stringent biosafety standards. This investigation demonstrates that mRNA/Man-LNP can trigger both humoral and cellular immune responses, suggesting its potential as a potent and promising vaccine candidate for controlling African swine fever (ASF).
研究领域:
兽医学
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免疫学
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分子生物学
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病毒学
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DOI
PubMed
高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2025
·
IF 11.5
Zhou Ye,Manman Zhu,Shaojie Li,Fan Zhang,Yingqi Ran,Cong Liu,Xiangchang Xu,Shujiao Liu,Xiang Xie,Yingchen Wang,Lan Yao
Cardiac autoimmune injury and oxidative stress play critical roles in the development of myocarditis. Promising approaches for treating this condition include suppressing excessive immune responses and reducing oxidative stress in the myocardium. The programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) axis is known to regulate immune responses and prevent damage caused by T-cell overactivation, while elevated reactive oxygen species (ROS) contribute to the progression of myocarditis. In this study, we developed multifunctional nanoparticles (PMN@EDR) that overexpress PD-L1 and are loaded with edaravone (EDR). The PMN@EDR NPs were successfully synthesized and comprehensively characterized. PMN@EDR effectively targeted inflammation-stimulated CD4 + T cells and damaged myocardial cells, inhibiting CD4 + T-cell proliferation, activation, and the release of pro-inflammatory cytokines via the PD-1/PD-L1 pathway. Additionally, PMN@EDR further suppressed CD4 + T-cell activation and alleviated HL-1 cardiomyocyte damage by releasing EDR to eliminate free radicals. For the in vivo treatment of myocarditis, compared to traditional single-target anti-inflammatory and antioxidant drugs, PMN@EDR not only reduced inflammation and the release of inflammatory mediators but also decreased ROS levels, thereby minimizing cardiomyocyte apoptosis and improving cardiac function. In conclusion, the PMN@EDR-based modulation of immune responses and oxidative stress offers a promising therapeutic strategy for myocarditis.
研究领域:
纳米技术
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免疫学
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心脏病学
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药理学
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产品关联
DOI
PubMed
高影响因子
CELL
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2019
·
IF 36.216
Ke-qi Fan,Yi-yuan Li,Hao-li Wang,Xin-tao Mao,Jin-xin Guo,Fei Wang,Ling-jie Huang,Yi-ning Li,Xiang-yu Ma,Zheng-jun Gao,Wei Chen,Dan-dan Qian,Wen-jin Xue,Qian Cao,Lei Zhang,Li Shen,Long Zhang,Chao Tong,Jiang-yan Zhong,Wei Lu,Ling Lu,Ke-ming Ren,Guisheng Zhong,Yuan Wang,Mingliang Tang,Xin-Hua Feng,Ren-jie Chai,Jin Jin
Summary Physical or mental stress leads to neuroplasticity in the brain and increases the risk of depression and anxiety. Stress exposure causes the dysfunction of peripheral T lymphocytes. However, the pathological role and underlying regulatory mechanism of peripheral T lymphocytes in mood disorders have not been well established. Here, we show that the lack of CD4 + T cells protects mice from stress-induced anxiety-like behavior. Physical stress-induced leukotriene B4 triggers severe mitochondrial fission in CD4 + T cells, which further leads to a variety of behavioral abnormalities including anxiety, depression, and social disorders. Metabolomic profiles and single-cell transcriptome reveal that CD4 + T cell-derived xanthine acts on oligodendrocytes in the left amygdala via adenosine receptor A1. Mitochondrial fission promotes the de novo synthesis of purine via interferon regulatory factor 1 accumulation in CD4 + T cells. Our study implicates a critical link between a purine metabolic disorder in CD4 + T cells and stress-driven anxiety-like behavior.
研究领域:
免疫学
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神经科学
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分子生物学
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行为科学
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DOI
PubMed
高影响因子
ACS Nano
·
2024
·
IF 15.8
Wenjuan Ma,Junyi Che,Weiwei Chen,Dandan Wang,Huayong Zhang,Yuanjin Zhao
The therapeutic application of mesenchymal stem cells (MSCs) has good potential as a treatment strategy for systemic lupus erythematosus (SLE), but traditional MSC therapy still has limitations in effectively modulating immune cells. Herein, we present a promising strategy based on dexamethasone liposome-integrated MSCs (Dexlip-MSCs) for treating SLE via multiple immunomodulatory pathways. This therapeutic strategy prolonged the circulation time of dexamethasone liposomes in vivo, restrained CD4+T-cell proliferation, and inhibited the release of proinflammatory mediators (IFN-γ and TNF-α) by CD4+T cells. In addition, Dexlip-MSCs initiated cellular reprogramming by activating the glucocorticoid receptor (GR) signaling pathway to upregulate the expression of anti-inflammatory factors such as cysteine-rich secretory protein LCCL-containing domain 2 (CRISPLD2) and downregulate the expression of proinflammatory factors. In addition, Dexlip-MSCs synergistically increased the anti-inflammatory inhibitory effect of CD4+T cells through the release of dexamethasone liposomes or Dex-integrated MSC-derived exosomes (Dex-MSC-EXOs). Based on these synergistic biological effects, we demonstrated that Dexlip-MSCs alleviated disease progression in MRL/lpr mice more effectively than Dexlip or MSCs alone. These features indicate that our stem cell delivery strategy is a promising therapeutic approach for clinical SLE treatment.
研究领域:
免疫学
·
干细胞治疗
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风湿病学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2024
·
IF 5.7
Zongping Zhu,Yirong Luo,Liting Lin,Tianhui Gao,Qingsong Yang,Yunqiu Fan,Shuyi Wang,Chaomei Fu,Wan Liao
Turmeric, a traditional medicinal herb, is commonly used as a dietary and functional ingredient. This study aimed to investigate the effect of turmeric polysaccharides (TPs) on intestinal immunity and gut microbiota in cyclophosphamide (Cy)-induced immunosuppressed BALB/c mice. We verified that the oral administration of TPs-0 and TPs-3 (200 and 400 mg/kg, bw) improved thymus and spleen indexes, increased the whole blood immune cells (WBC) and lymph count index, and stimulated the secretion of serum immunoglobulin IgG. More importantly, TPs-0 and TPs-3 could repair intestinal immune damage and reduce intestinal inflammation. The specific mechanism is ameliorating the intestinal pathological damage, promoting CD4+ T cell secretion, regulating the expression of related cytokines, and reducing the level of critical proteins in the NF-κB/iNOS pathway. Interestingly, the intake of TPs-0 and TPs-3 significantly increased the content of short-chain fatty acids (SCFAs). Moreover, TPs-0 and TPs-3 relieved the intestinal microbiota disorder via the proliferation of the abundance of Lactobacillus and Bacteroides and the inhibition of Staphylococcus. Cumulatively, our study suggests that TPs-0 and TPs-3 can relieve intestinal immune damage by repairing the immune barrier and regulating intestinal flora disorders. TPs have potential applications for enhancing immunity as a functional food.
研究领域:
免疫学
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微生物学
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药理学
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营养科学
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产品关联
DOI
PubMed
高影响因子