JOURNAL OF NUTRITION
·
2023
·
IF 4.2
Luyuan Kang,Jiaman Pang,Xiangyu Zhang,Yisi Liu,Yujun Wu,Junjun Wang,Dandan Han
Background L-arabinose has anti-inflammatory and metabolism-promoting properties, and macrophages participate in the alleviation of inflammation; however, the mechanism by which they contribute to the anti-inflammatory effects of L-arabinose is unknown. Objectives To investigate the involvement of macrophages in the mitigation of L-arabinose in an intestinal inflammation model induced by lipopolysaccharide (LPS). Methods Five-week-old male C57BL/6 mice were divided into 3 groups: a control and an LPS group that both received normal water supplementation, and an L-arabinose (ARA+LPS) group that received 5% L-arabinose supplementation. Mice in the LPS and ARA+LPS groups were intraperitoneally injected with LPS (10 mg/kg body weight), whereas the control group was intraperitoneally injected with the same volume of saline. Intestinal morphology, cytokines, tight junction proteins, macrophage phenotypes, and microbial communities were profiled at 6 h postinjection. Results L-arabinose alleviated LPS-induced damage to intestinal morphology. L-arabinose down-regulated serum tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6, and messenger RNA (mRNA) levels of TNF-α , IL-1β , interferon-γ ( IFN-γ ), and toll-like receptor-4 in jejunum and colon compared with those of the LPS group ( P < 0.05). The mRNA and protein levels of occludin and claudin-1 were significantly increased by L-arabinose ( P < 0.05). Interferon regulatory factor-5 ( IRF-5 ) and signal transducer and activator of transcription-1 ( STAT-1 ), key genes characterized by M1 macrophages, were elevated in the jejunum and colon of LPS mice ( P < 0.05) but decreased in the ARA+LPS mice ( P < 0.05). In vitro , L-arabinose decreased the proportion of M1 macrophages and inhibited mRNA levels of TNF-α , IL-1β , IL-6 , IFN-γ , as well as IRF-5 and STAT-1 ( P < 0.01). Moreover, L-arabinose restored the abundance of norank_ f__Muribaculaceae , Faecalibaculum , Dubosiella , Prevotellaceae_UCG-001 , and Paraasutterella compared with those of LPS ( P < 0.05) and increased the concentration of short-chain fatty acids ( P < 0.05). Conclusion The anti-inflammatory effects of L-arabinose are achieved by reducing M1 macrophage polarization, suggesting that L-arabinose could be a candidate functional food or nutritional strategy for intestinal inflammation and injury.
研究领域:
免疫学
·
胃肠病学
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营养学
·
微生物学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2024
·
IF 7.7
Wanyu Li,Qingbang Ye,Zhonghao Jiang,Dong Xia,Zhuo Yan,Dan Wang,Yanan Chen,Tianshou Cao,Jilong Wang,Chihao Lin,Huiling Yang,Junjie Deng,Jiantao Lin
Pro-inflammatory M1 macrophages possess the ability to change the immunosuppressive tumor microenvironment by releasing various inflammatory factors simultaneously, which can effectively inhibit tumor progression and relapse. Promoting macrophage polarization towards M1 may be an effective way to treat Melanoma. However, the risk of cytokine storm caused by the proliferation and excessive activation of M1 macrophages greatly limits it as a biosafety therapeutic strategy in anti-tumor immunotherapy. Therefore, how to engineer natural M1 macrophage to a biocompatible biomaterial that maintains the duration time of tumor suppressive property duration time still remains a huge challenge. To achieve this goal, we developed an injectable macroporous hydrogel (M1LMHA) using natural M1 macrophage lysates and alginate as raw materials. M1LMHA had excellent biocompatibility, adjustable degradation rate and could sustainably release varieties of natural inflammatory factors, such as tumor necrosis factor-α (TNF-α), interferon-gamma (IFN-γ), and interleukin-12 (IL-12), etc. M1LMHA could repolarize anti-inflammatory M2 macrophages to M1 macrophages by the synergistic effect of released tiny inflammatory factors via the NF-κB pathway. This study supported that M1LMHA might be an effective and safe tool to activate tumor-associated immune cells, improving the efficiency of anti-tumor immunotherapy.
研究领域:
生物材料学
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免疫学
·
肿瘤学
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产品关联
DOI
PubMed
高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
·
2024
·
IF 4.2
Haocong Zhang,Liangbi Xiang,Hong Yuan,Hailong Yu
Spinal cord injury (SCI) is a severe central nervous system injury and microglia are major participants in neuroinflammation after injury. ADP-ribosylation factor-like GTPase 11 (ARL11) is a GTP-binding protein. Whether ARL11 is involved in the SCI progression is unknown. In the impactor-induced moderate SCI mouse model, ARL11 protein and mRNA expression were significantly increased in the injury site. LPS (100 ng/mL) and IFN-γ (20 ng/mL) were incubated with BV2 cells (immortalized mouse microglial cell line) to drive them into an M1-like phenotype. ARL11 up-regulation was also observed in activated microglia in SCI mice and LPS and IFN-γ treated BV2 cells. Basso Mouse Scale scores and inclined plate test revealed that ARL11 deletion promoted motor function recovery in SCI mice. Pathological examination showed ARL11 knockdown reduced spinal cord tissue damage, increased neuron numbers, and inhibited neuronal apoptosis in SCI mice. ARL11 knockdown notably inhibited IL-1β and IL-6 production in vivo and in vitro. Furthermore, ARL11 deletion significantly inhibited iNOS protein and mRNA expression in vivo and in vitro, and COX-2 expression in vivo . Mechanism studies revealed that ARL11 silencing decreased phosphorylated ERK1/2 protein expression. Additionally, ELF1 knockdown significantly inhibited ARL11 protein and mRNA expression in vitro . ELF1 acted as a transcription activator in regulating ARL11 expression by binding to the promoter. In conclusion, ARL11 knockdown protects neurons by inhibiting M1 microglia-induced neuroinflammation, thereby promoting motor functional recovery in SCI mice. This may occur in part under the regulation of ELF1. Our study provides a new molecular target for SCI treatment.
研究领域:
神经科学
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炎症
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分子生物学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
·
2025
·
IF 2.8
Yunbing Chen,Xinping Li,Hongyi Yang,Gaoying Ran,Lifang Zhang,Shuguang Zeng
β-Tricalcium phosphate (β-TCP), frequently employed for bone tissue regeneration, can induce inflammation during the initial phases of implantation within the organism. However, mechanisms by which β-TCP nanoparticles (NPs) cause this inflammatory response is rarely reported. This project aims to investigate the causes of the macrophage inflammatory response induced by β-TCP NPs. Here, macrophage-like RAW264.7 cells were co-cultured with conditioned medium containing β-TCP NPs to identify the pathways through which β-TCP NPs influence inflammation and polarization of macrophages. This effect is achieved by modulating mitochondrial oxidative stress in the immune microenvironment. The results demonstrated that β-TCP NPs caused mitochondrial swelling, increased intracellular calcium ions, reduced mitochondrial membrane potential, as well as decreased the level of adenosine triphosphate (ATP) and translocase of outer mitochondrial membrane 20 (TOMM20). These NPs further lead to mitochondrial oxidative damage. These alterations promoted the polarization of macrophage to M1-type. Exogenous mitochondrial-targeted antioxidants could block this M1-type macrophage polarization. The findings of this work suggest that β-TCP NPs induce macrophage inflammation and contribute to M1 macrophage polarization, primarily through the activation of mitochondrial oxidative stress. These insights could guide the development of improved β-TCP formulations to mitigate inflammatory responses in bone regeneration applications.
研究领域:
生物材料学
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免疫学
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纳米医学
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骨生物学
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分子细胞生物学
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转化医学
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产品关联
DOI
PubMed
高影响因子
Journal of Biomedical Nanotechnology
·
2024
·Vol. 20
·期 8
·1307-1314
·
IF 2.9
Zhu Yunhan,Chen Renshou
Sepsis-induced Acute kidney injury (SA-AKI), a common complication in sepsis, significantly impacts patients’ health and quality of life. M1 macrophages have been demonstrated to release inflammatory mediators that exacerbate kidney injury. MiR-155 has been implicated in promoting
inflammation and damage during sepsis while reducing miR-155 levels alleviates SA-AKI. However, the relationship between miR-155 and M1 macrophage-derived exosomes in regulating autophagy during SA-AKI remains unclear. In this study, we aim to investigate the relationship between M1 macrophage-derived
exosomes and miR-155 in regulating autophagy during SA-AKI. A mouse model of SA-AKI was established by performing cecal ligation and puncture (CLP) surgery. Additionally, the HK-2 cell line was utilized to establish a sepsis cell model by inducing lipopolysaccharide (LPS). We demonstrated
that the mice model of SA-AKI exhibited renal injury along with enhanced autophagy, inflammation response, and macrophage polarization after CLP surgery. M1 macrophages attenuated cell viability and enhanced autophagy in LPS-treated HK-2 cells. Additionally, M1 macrophage-derived exosomes
were observed to enhance autophagy in LPS-treated HK-2 cells. Furthermore, we confirmed an increased expression of miR-155 in M1 macrophage-derived exosomes. Furthermore, exosome-mediated miR-155 enhanced autophagy in LPS-treated HK-2 cells. In conclusion, this study provides the first evidence
that exosomal miR-155 derived from M1 macrophages enhances autophagy in SA-AKI. These findings suggest that targeting exosomal miR-155 could be a promising therapeutic strategy for SA-AKI.
研究领域:
免疫学
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肾病学
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分子生物学
·
重症医学
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DOI
高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2022
·
IF 11.467
Jianing Zhao,Longbing Ling,Wei Zhu,Tianhao Ying,Tao Yu,Mengmeng Sun,Xuan Zhu,Yuan Du,Leiming Zhang
Atherosclerosis (AS), a leading cause of death worldwide, involves chronic macrophage inflammation from its initiation to the emergence of complications. Targeting plaque inflammation by re-polarizing pro-inflammatory M1 to anti-inflammatory M2 could therefore provide a promising strategy to treat AS, but currently available anti-inflammatory drugs limit clinical outcomes. In this study, we found that kaempferol (KPF) is capable of potential anti-inflammation as a novel drug candidate, which has been scarcely reported. Building upon these findings, we fabricated a macrophage-biomimetic KPF delivery platform, abbreviated as [email protected] to potentiate therapeutic payloads, wherein the designed ROS-responsive Dextran- g -PBMEO NPs with π-π stacking were coated with macrophage membrane (MM) for effective target and accumulation in atherosclerotic lesions. Therapy of [email protected] afforded significant decrease in proliferating macrophage inflammation while went with the reduction of key pro-inflammatory cytokines and re-polarization M1 to M2 phenotype, inducing excellent anti-AS responses in ApoE −/− mice after i.p. delivery. The mechanism of [email protected] was further investigated and found it related to block the ROS/NF-κB signaling pathways. Together with as well demonstrated biosafety profiles, this proof-of-concept opens an instructive door for the study of KPF-mediated nanodrugs in treatment of AS based on biomimetic NPs.
研究领域:
药理学
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纳米技术
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心血管疾病
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炎症
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药物递送系统
✓ 已验证
产品关联
DOI
PubMed
高影响因子
FOOD CONTROL
·
2014
·
IF 2.819
Daofeng Liu,Yanmei Huang,Shuying Wang,Kun Liu,Minghui Chen,Yonghua Xiong,Wanchun Yang,Weihua Lai
A modified lateral flow immunoassay (two-step assay) was developed to detect trace aflatoxin M1 (AFM1) in raw milk. In contrast to conventional LFIA, two kinds of immunomagnetic nanobeads (IMNBs) were used. One IMNB with high antibody concentration was used to capture AFM1 in the test sample, whereas the other IMNB with low antibody concentration was used to elucidate the results of the test. Critical factors, such as antibody concentration of IMNBs and size of IMNBs, were investigated. The two-step assay exhibited an ideal sensitivity to screen trace AFM1 in milk samples without extra sample pretreatment. The cutoff value of the naked eye was 0.02 μg/L and satisfied the European Union's maximum limit of AFM1 in raw milk, heat-treated milk, and milk used to manufacture milk-based products and even in baby foods. With the same antibody, sensitivity was enhanced approximately 25 and 50 times when compared with conventional IMNB-based LFIA and gold-based LFIA, respectively. Corresponding results of 13 raw milk samples were obtained between this two-step assay and referenced enzyme-linked immunosorbent assay.
研究领域:
食品科学
·
免疫学
✓ 已验证
产品关联
DOI
高影响因子
Frontiers in Immunology
·
2021
·
IF 7.561
Li Qiuju,Yuan Ming,Jiao Xue,Huang Yufei,Li Jing,Li Dong,Ji Miaomiao,Wang Guoyun
Background: Endometriosis is a common nonmalignant gynecological disorder that affects 10–15% women of reproductive age and causes several symptoms that result in decreased quality of life and a huge social burden. In recent decades, extracellular vesicles (EVs) have gained attention as a potential therapeutic tool; however, the therapeutic effects of EVs against endometriosis have not been reported. Accordingly, in this study, we investigated the feasibility of nanovesicles (NVs) derived from M1 macrophages (M1NVs) in treating endometriosis.Methods: M1NVs were prepared by serial extrusion. Co-culture assays were performed to investigate changes in tube formation and migration/invasion of eutopic endometrial stroma cells (ESCs) obtained from patients with endometriosis (EM-ESCs). A mouse model of endometriosis was established, and mice were treated with phosphate-buffered saline, M0NVs, or M1NVs to evaluate the efficacy and safety of M1NV for treating endometriosis.Results: M1NVs directly or indirectly inhibited the migration and invasion of EM-ESCs and reduced tube formation. In the mouse model, M1NVs suppressed the development of endometriosis through reprogramming of M2 macrophages, without causing damage to the organs.Conclusions: M1NVs inhibit the development of endometriosis directly, or through repolarizing macrophages from M2 to M1 phenotype. Hence, administration of M1NVs may represent a novel method for the treatment of endometriosis.
研究领域:
妇科学
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免疫学
·
纳米技术
·
细胞生物学
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产品关联
DOI
PubMed
高影响因子
3 Biotech
·
2021
·Vol. 11
·期 12
·1-13
·
IF 2.406
Tang Miaolong,Cai Jimin,Wang Yan,Huan Zhirong,Yao Hao,Xu Ce,Ge Xin,Song Sheng
Hemorrhage shock (HS) is a major threat to patients with trauma and spontaneous bleeding, resulting in multi-organ failure including the kidney. Tyrosine kinase nonreceptor 1 (TNK1) has been shown to be upregulated in the kidney of experimental HS and patients with severe trauma . The study aims to investigate the role of TNK1 and the underlying mechanism in HS-induced kidney injury. A model of HS was established with femoral artery bloodletting, followed by resuscitation in Sprague–Dawley rats. Renal expression of TNK1 was abnormally induced by HS in rats. Knockdown of TNK1 alleviated HS-induced cell apoptosis and the level of proinflammatory cytokines (TNF-α, IL-6 and IL-1β) in the kidney. The expression of M1 macrophage markers (CD86 and iNOS) and the activation of STAT1 were inhibited by TNK1 knockdown in HS rats. In vitro, human monocyte THP-1 cells were treated with 20 ng/mL interferon-gamma plus 100 ng/mL lipopolysaccharide to induce M1 polarization. TNK1 knockdown exerted inhibitory effect on macrophage M1 polarization, M1-type inflammatory cytokine production and STAT1 activation in THP-1 cells. In conclusion, downregulation of TNK1 alleviates HS-induced kidney injury by suppressing macrophage M1 polarization, inflammation and kidney cell apoptosis, in which the deactivation of STAT1 signaling may be involved.
研究领域:
医学
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免疫学
·
分子生物学
✓ 已验证
DOI
PubMed
高影响因子
BIOELECTROCHEMISTRY
·
2023
·
IF 5
Wenjing Qian,Jingming Zhou,Yumei Chen,Hongliang Liu,Peiyang Ding,Yankai Liu,Chao Liang,Xifang Zhu,Ying Zhang,Enping Liu,Aiping Wang,Gaiping Zhang
Virginiamycin (VIR), a feed additive, is used to promote pig and poultry growth. However, it is hazardous to human health. This work described a label-free electrochemical immunosensor based on silver nanoparticles-reduced graphene oxide (AgNPs-rGO) nanocomposites and staphylococcal protein A (SPA) for the first time to directly detect the residual marker VIR M1. Good catalytic currents for oxygen reduction reaction were apparently obtained after the modification of nanocomposites on gold electrode. Nanocomposites were characterized using UV–Vis, X-ray diffraction (XRD) patterns, Fourier transform infrared spectroscopy (FTIR) and transmission electron microscopy (TEM). SPA was targeted to immobilize VIR M1 monoclonal antibody (mAb) by binding to Fc region of antibody. The proposed immunosensor showed a wide linear range from 0.25 ng mL −1 to 100 ng mL −1 , providing detection limit (LOD) of 0.18 ng mL −1 of VIR M1. Recovery rates ranged from 92.27% to 98.84%, and relative standard deviation (RSD) was not above 6.6%, indicating the immunosensor could detect VIR M1 in actual samples with high accuracy. The sensor showed good selectivity, reproducibility and stability and could be considered as a potential tool for detection of VIR M1 in feed and animal derived food.
研究领域:
分析化学
·
电化学
·
生物传感器
·
食品安全
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Advanced Science
·
2025
·
IF 14.1
Caifeng Deng,Yongbing Xiao,Xuan Zhao,Hui Li,Yuxiao Chen,Kelong Ai,Ting Jiang,Jie Wei,Xiaoyuan Chen,Guanghua Lei,Chao Zeng
The infiltration and excessive polarization of M1 macrophages contribute to the induction and persistence of low-grade inflammation in joint-related degenerative diseases such as osteoarthritis (OA). The lipid metabolism dysregulation promotes M1 macrophage polarization by coordinating the compensatory pathways of the inflammatory and oxidative stress responses. Here, a self-assembling, licofelone-loaded nanoparticle (termed LCF-CSBN), comprising chondroitin sulfate and bilirubin joined by an ethylenediamine linker, is developed to selectively reprogram lipid metabolism in macrophage activation. LCF-CSBN is internalized by M1 macrophages via CD44-mediated endocytosis and targets the Golgi apparatus accompanied with the reactive oxygen species-responsive release of licofelone (LCF, dual inhibitor of arachidonic acid metabolism). LCF-CSBN effectively promotes M1 to M2 macrophage transition by reprogramming the Golgi apparatus-related sphingolipid metabolism and arachidonic acid metabolism. Intra-articularly injected LCF-CSBN retains in the joint for up to 28 days and accumulates into M1 macrophages. Moreover, LCF-CSBN can effectively attenuate joint inflammation, oxidative stress, and cartilage degeneration in OA model rats. These findings indicate the promising potential of lipid-metabolism-reprogramming LCF-CSBN in the targeted therapy of OA.
研究领域:
药理学
·
免疫学
·
骨科
·
纳米技术
·
代谢
✓ 已验证
产品关联
DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
·
IF 4.8
Ran Sun,Yan-Fang Wang,Xue Yang
The key to the treatment of multiple sclerosis (MS) is to promote the transition from inflammation-induced demyelination to remyelination. Polarization of microglia towards M1 or M2 phenotype is critical in this transition. Interferon induced protein with tetratricopeptide repeats 3 (IFIT3) is involved in inflammatory reaction and up-regulated in M1-polarized macrophages. However, its effect on microglia during MS has not been reported. In this paper, we demonstrated the important role of IFIT3 in selectively regulating microglia polarization. The expression of IFIT3 was increased when microglia were polarized towards M1, but did not change under M2 polarization. The knockdown of IFIT3 selectively inhibited M1 polarization, while M2 polarization was not affected by IFIT3 silencing. Furthermore, the activation of signal transducer and activator of transcription 1 (STAT1) and nuclear factor kappa-B (NF-ĸB) signaling in M1 polarized microglia was suppressed by downregulating IFIT3. In experimental autoimmune encephalitis (EAE) mice, an animal model of MS, IFIT3 expression was upregulated. The disease progression, inflammatory infiltration and demyelination in the EAE mice were alleviated by silencing IFIT3. The inhibitory effects of IFIT3 knockdown on M1 polarization and STAT1 and NF-ĸB pathways were also confirmed in the spinal cord of EAE mice. In summary, our findings suggest that IFIT3 selectively intensified microglia polarization towards the pro-inflammatory M1 phenotype, and may contribute to the progression of MS.
研究领域:
神经科学
·
免疫学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）