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| 1 | The omentum显示文摘INTRODUCTIONThe word omentum derives from the ancientEgyptians who,when embalming human bodies,used to assess their'omens'by looking at thevariations in what we recognise today as theomentum.Galen(128-199 AD)thought that therole of the omentum was to warm the intestines.This was on the basis of a gladiator who had anomental resection after a stab injury and sufferedgreatly from cold for the rest of his life.A | Cameron Platell Deborah Cooper John M.Papadimitriou John C.Hall | 2000 | World Journal of Gastroenterology2000，6，2： | 57 |
| 2 | Lipid homeostasis and the formation of macrophage-derived foam cells in atherosclerosis显示文摘Atherosclerosis is a chronic,inflammatory disorder characterized by the deposition of excess lipids in the arterial intima.The formation of macrophage-derived foam cells in a plaque is a hallmark of the development of atherosclerosis.Lipid homeostasis,especially cho-lesterol homeostasis,plays a crucial role during the formation of foam cells.Recently,lipid droplet-associated proteins,including PAT and CIDE family proteins,have been shown to control the development of athero-sclerosis by regulating the formation,growth,stabiliza-tion and functions of lipid droplets in macrophage-derived foam cells.This review focuses on the potential mechanisms of formation of macrophage-derived foam cells in atherosclerosis with particular emphasis on the role of lipid homeostasis and lipid droplet-associated proteins.Understanding the process of foam cell for-mation will aid in the future discovery of novel thera-peutic interventions for atherosclerosis. | Yuan Yuan Peng Li Jing Ye | 2012 | Protein & Cell2012，3，3： | 44 |
| 3 | Myeloid immunosuppression and immune checkpoints in the tumor microenvironment显示文摘Tumor-promoting inflammation and the avoidance of immune destruction are hallmarks of cancer.While innate immune cells,such as neutrophils,monocytes,and macrophages,are critical mediators for sterile and nonsterile inflammation,persistent inflammation,such as that which occurs in cancer,is known to disturb normal myelopoiesis.This disturbance leads to the generation of immunosuppressive myeloid cells,such as myeloid-derived suppressor cells(MDSCs)and tumor-associated macrophages(TAMs).Due to their potent suppressive activities against effector lymphocytes and their abundance in the tumor microenvironment,immunosuppressive myeloid cells act as a major barrier to cancer immunotherapy.Indeed,various therapeutic approaches directed toward immunosuppressive myeloid cells are actively being tested in preclinical and clinical studies.These include antiinflammatory agents,therapeutic blockade of the mobilization and survival of myeloid cells,and immunostimulatory adjuvants.More recently,immune checkpoint molecules expressed on tumor-infiltrating myeloid cells have emerged as potential therapeutic targets to redirect these cells to eliminate tumor cells.In this review,we discuss the complex crosstalk between cancer-related inflammation and immunosuppressive myeloid cells and possible therapeutic strategies to harness antitumor immune responses. | Kyohei Nakamura Mark J.Smyth | 2020 | Cellular & Molecular Immunology2020，17，1： | 31 |
| 4 | Extracellular vesicle activities regulating macrophage- and tissue-mediated injury and repair responses显示文摘Macrophages are typically identified as classically activated(M1) macrophages and alternatively activated(M2) macrophages,which respectively exhibit pro-and anti-inflammatory phenotypes,and the balance between these two subtypes plays a critical role in the regulation of tissue inflammation,injury,and repair processes.Recent studies indicate that tissue cells and macrophages interact via the release of small extracellular vesicles(EVs) in processes where EVs released by stressed tissue cells can promote the activation and polarization of adjacent macrophages which can in turn release EVs and factors that can promote cell stress and tissue inflammation and injury and vice versa.This review discusses the roles of such EVs in resulating such interactions to influence tissue inflammation and injury in a number of acute and chronic inflammatory disease conditions,and the potential applications,advantage and concerns for using EV-based therapeutic approaches to treat such conditions,including their potential role of drug carriers for the treatment of infectious diseases. | Qian Hu Christopher J.Lyon Jesse K.Fletcher Wenfu Tang Meihua Wan Tony Y.Hu | 2021 | Acta Pharmaceutica Sinica B2021，11，6： | 22 |
| 5 | Lp-PLA2 inhibition prevents Ang Ⅱ-induced cardiac inflammation and fibrosis by blocking macrophage NLRP3 inflammasome activation显示文摘Macrophage-mediated inflammation plays an important role in hypertensive cardiac remodeling,whereas effective pharmacological treatments targeting cardiac inflammation remain unclear.Lipoprotein-associated phospholipase A2(Lp-PLA2)contributes to vascular inflammation-related diseases by mediating macrophage migration and activation.Darapladib,the most advanced Lp-PLA2 inhibitor,has been evaluated in phase Ⅲ trials in atherosclerosis patients.However,the role of darapladib in inhibiting hypertensive cardiac fibrosis remains unknown.Using a murine angiotensin Ⅱ(Ang Ⅱ)infusion-induced hypertension model,we found that Pla2g7(the gene of Lp-PLA2)was the only upregulated PLA2 gene detected in hypertensive cardiac tissue,and it was primarily localized in heart-infiltrating macrophages.As expected,darapladib significantly prevented Ang Ⅱ-induced cardiac fibrosis,ventricular hypertrophy,and cardiac dysfunction,with potent abatement of macrophage infiltration and inflammatory response.RNA sequencing revealed that darapladib strongly downregulated the expression of genes and signaling pathways related to inflammation,extracellular matrix,and proliferation.Moreover,darapladib substantially reduced the Ang Ⅱ infusion-induced expression of nucleotide-binding oligomerization domain-like receptor with pyrin domain 3(NLRP3)and interleukin(IL)-1β and markedly attenuated caspase-1 activation in cardiac tissues.Furthermore,darapladib ameliorated Ang Ⅱ-stimulated macrophage migration and IL-1β secretion in macrophages by blocking NLRP3 inflammasome activation.Darapladib also effectively blocked macrophage-mediated transformation of fibroblasts into myofibroblasts by inhibiting the activation of the NLRP3 inflammasome in macrophages.Overall,our study identifies a novel anti-inflammatory and anti-cardiac fibrosis role of darapladib in Lp-PLA2 inhibition,elucidating the protective effects of suppressing NLRP3 inflammasome activation.Lp-PLA2 inhibition by darapladib represents a novel therapeutic strategy for hypertensive cardiac damage treatment. | Si-lin Lv Zi-fan Zeng Wen-qiang Gan Wei-qi Wang Tie-gang Li Yu-fang Hou Zheng Yan Ri-xin Zhang Min Yang | 2021 | Acta Pharmacologica Sinica2021，42，12： | 21 |
| 6 | Serum and ascites levels of macrophage migration inhibitory factor, TNF-α and IL-6 in patients with chronic virus hepatitis B and hepatitis cirrhosis显示文摘Objective: To study the potential role of macrophagemigration inhibitory factor (MIF), tumor necrosisfactor-α (TNF-α) and interleukin-6 (IL-6) in thedevelopment of chronic virus hepatitis B (CH) andhepatitis cirrhosis (HC).Methods: The serum concentrations of MIF, TNF-αand IL-6 in 18 patients with chronic virus hepatitis Band in 14 patients with hepatitis cirrhosis without as-citic fluid, and the serum and ascites cytokine con-centrations in 22 HC patients with ascitic fluid weredetected by enzyme linked immunity sorbed assay.Results: The cytokine concentrations of the patientswere significantly higher than those of the controls.The serum levels of MIF, TNF-α and IL-6 of the 22patients with ascitic fluid were higer than those of 14HC patients without ascites. In the 18 patients withCH, the serum cytokine concentrations were the low-est. The serum cytokine concentrations of the 22 HCpatients with ascites were significantly higher thanthose of the 14 HC patients without ascites (P<0. 01). Their serum cytokine concentrations were sig-nificantly higher than those in the 18 patients withCH (P<0. 01). The concentration of IL-6 in asciteswas the highest among all the groups. The serum le-vels of MIF, TNF-α and IL-6 are correlated with al-anine aminotransferase (ALT) in the patients withCH, but not in those with HC with or without asci-tes.Conclusions: These results indicated that MIF, TNF-α and IL-6 may participate in the pathologicalprocess of CH and cirrhosis, that IL-6 seems to playan important role in ascites formation, and that se-rum levels of MIF, TNF-α and IL-6 appear to reflectthe severity of tissue injury in HBV disease. | Wei Zhang Bei Yue Gui-Qiang Wang Shu-Lan Lu the Department of Infectious Dispeases, Ruijing Hospital, Shanghai Second Medical University, Shanghai 200025, China Department of Intectious Diseases, Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China | 2002 | Hepatobiliary & Pancreatic Diseases International2002，1，4： | 18 |
| 7 | Effect and molecular mechanism of mir-146a on proliferation of lung cancer cells by targeting and regulating MIF gene显示文摘Objective: To discuss the effect and molecular mechanism of mi R-146 a on the proliferation of lung cancer cells by targeting and regulating the macrophage migration inhibitory factor(MIF) gene. Methods: RT-PCR was employed to detect expression of mi R-146a; immunohistochemistry was used to detect the expression of MIF. The luciferase reporter gene technique was adopted to verify that MIF was the specific reverse target gene of mi R-146 a and the liposome LipofectamineTM2000 was employed to transfer the modeled mi R-146 a mimics, and mi R-146 a negative control(NC) in NSCLC cells to detect the expression of MIF m RNA and protein. MTT assay was used to detect cell viability, cloning technique to detect cell proliferation ability, Annexin V-PI to detect cell apoptosis, UV spectrophotometry to detect viability of cysteinyl aspartate specific proteinase 3(Caspase 3), and western blot to detect expression of nuclear factor-κB(NF-κB) in cells. Results: The expression of mi R-146 a in NSCLC lung tissues was lower than that in the normal lung tissues besides the lung cancer; while the expression of mi R-146 a in NSCLC cells was lower than that in normal human embryonic lung tissues. It was chosen as the subsequent cell line for its appropriate expression in A549. The expression of MIF protein in NSCLC lung tissues was higher than that in the normal lung tissues besides the lung cancer. The luciferase reporter gene proved that MIF was the reverse target gene of mi R-146 a. The mi R-146 a mimics were transfected into A549 cells through the liposome. Compared with NC group, the expression of MIF protein and m RNA was significantly decreased(P<0.01), with the decrease in the cell viability(P<0.01), the decrease in the number of clones(P<0.01), cell apoptosis(P<0.01), the increase in the activity of Caspase 3(P<0.01), and decrease in the phosphorylation of NF-κB p65(P<0.01). Conclusions: mi R-146 a has low expression in NSCLC tissues and cell lines, while MIF has the over expression in NSCLC tissues. The increased expression of mi R-146 a can inhibit the expression of MIF via the gene targeting and thus inhibit the proliferation of A549 cells and induce the apoptosis of cancer cells, which may be realized through NF-κB signaling pathway. | Wu-Ming Wang Ji-Chun Liu | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，8： | 17 |
| 8 | Inflammatory response of macrophages in infection显示文摘BACKGROUND: Macrophages are widely-distributed innate immune cells playing diverse roles in various physiological and pathological processes. The primary function of macrophages is to phagocytize and clear invading pathogens.DATA SOURCES: A systematic search of PubMed was performed to identify relevant studies in English language literature using the key words such as macrophage and inflammation. A total of 122 articles related to inflammatory response of macrophages in infection were systematically reviewed.RESULTS: The inflammatory responses of macrophages triggered by infection comprise four interrelated phases:recognition of pathogen-associated molecular patterns by pattern-recognition receptors expressed on/in macrophages;enrichment of quantity of macrophages in local infected tissue by recruitment of circulating monocytes and/or in situ proliferation; macrophage-mediation of microbicidal activity and conversion to anti-inflammatory phenotype to terminate anti-infectious response and to promote tissue repair.Complicated regulation of macrophage activation at molecular level recognized in the past decade is also reviewed, including intracellular multiple signaling molecules, membrane molecules,microRNAs and even epigenetic-associated molecules.CONCLUSION: The inflammatory response of macrophages in infection is an orderly and complicated process under elaborate regulation at molecular level. | Ling Zhang Cheng-Cai Wang | 2014 | Hepatobiliary & Pancreatic Diseases International2014，13，2： | 17 |
| 9 | Broussonin E suppresses LPS-induced inflammatory response in macrophages via inhibiting MAPK pathway and enhancing JAK2-STAT3 pathway显示文摘Macrophages play an important role in inflammation, and excessive and chronic activation of macrophages leads to systemic inflammatory diseases, such as atherosclerosis and rheumatoid arthritis. In this paper, we explored the anti-inflammatory effect of broussonin E, a novel phenolic compound isolated from the barks of Broussonetia kanzinoki, and its underlying molecular mechanisms. We discovered that Broussonin E could suppress the LPS-induced pro-inflammatory production in RAW264.7 cells, involving TNF-α, IL-1β, IL-6, COX-2 and iNOS. And broussonin E enhanced the expressions of anti-inflammatory mediators such as IL-10, CD206 and arginase-1(Arg-1) in LPS-stimulated RAW264.7 cells. Further, we demonstrated that broussonin E inhibited the LPS-stimulated phosphorylation of ERK and p38 MAPK. Moreover, we found that broussonin E could activate janus kinase(JAK) 2, signal transducer and activator of transcription(STAT) 3. Downregulated pro-inflammatory cytokines and upregulated anti-inflammatory factors by broussonin E were abolished by using the inhibitor of JAK2-STAT3 pathway, WP1066. Taken together, our results showed that broussonin E could suppress inflammation by modulating macrophages activation state via inhibiting the ERK and p38 MAPK and enhancing JAK2-STAT3 signaling pathway, and can be further developed as a promising drug for the treatment of inflammation-related diseases such as atherosclerosis. | HUANG Shao-Peng GUAN Xin KAI Guo-Yin XU Ya-Zhou XU Yuan WANG Hao-Jie PANG Tao ZHANG Lu-Yong LIU Ying | 2019 | Chinese Journal of Natural Medicines2019，17，5： | 17 |
| 10 | IL-23-induced macrophage polarization and its pathological roles in mice with imiquimod-induced psoriasis显示文摘Macrophages acquire distinct phenotypes during tissue stress and inflammatory responses.Macrophages are roughly categorized into two different subsets named inflammatory M1 and anti-inflammatory M2 macrophages.We herein identified a unique pathogenic macrophage subpopulation driven by IL-23 with a distinct gene expression profile including defined types of cytokines.The freshly isolated resting mouse peritoneal macrophages were stimulated with different cytokines in vitro,the expression of cytokines and chemokines were detected by microarray,real-time PCR,ELISA and multiple colors flow cytometry.Adoptive transfer of macrophages and imiquimod-induced psoriasis mice were used.In contrast to M1-and M2-polarized macrophages,IL-23-treated macrophages produce large amounts of IL-17A,IL-22and IFN-γ.Biochemical and molecular studies showed that IL-23 induces IL-17A expression in macrophages through the signal transducer and activator of transcription 3(STAT3)-retinoid related orphan receptor-γ T (RORyT)pathway.T-bet mediates the IFN-γ production in IL-23-treated macrophages.Importantly,IL-23-treated macrophages signifi- cantly promote the dermatitis pathogenesis in a psoriasis-like mouse model.IL-23-treated resting macrophages express a distinctive gene expression prolife compared with M1 and M2 macrophages.The identification of IL-23-induced macrophage polarization may help us to understand the contribution of macrophage subpopulation in Th17-cytokines-related pathogenesis. | Yuzhu Hou Linnan Zhu Hongling Tian Hai-Xi Sun Ruoyu Wang Lianfeng Zhang Yong Zhao | 2018 | Protein & Cell2018，9，12： | 16 |
| 11 | Influence of whole peptidoglycan of bifidobacterium on cytotoxic effectors produced by mouse peritoneal macrophages显示文摘INTRODUCTIONBifidobacteria are physiologically beneficial bacteria which are perdominant in human intestine ,and possess the most important functions .They play an important role in maintaining microbial balance of the intestine .Furthermore , their presence is thought to be an important indication of health of the body [1-4].Whole peptidoglycan ( WPG) is the major component in the cell wall of bifidobacterium ,which is also a biological responsemodifier with nontoxic side dffcets. | Li Sheng Wang~1 Hui Ming Zhu~1 Dian Yuan Zhou~2 Yu Lin Wang~1 Wan Dai Zhang~2 ~1Departrnent of Gastroenterology,Shenzhen Municipal People’s Hospital,Jinan University of Medical Sciences,Shenzhen 518020,Guangdong Province,China ~2Chinese PLA Institute of Digestion,the First Military Medical University,Guangzhou 510515,Guangdong Province,ChinaLi Sheng Wang graduated and obtained Ph.D,from the First Military Medical University in 1998,now working at Department of Gastroenterology,Shenzhen Municipal People’s Hospital.Jinan University of Medical Sciences.having 35 papers published. | 2001 | World Journal of Gastroenterology2001，7，3： | 15 |
| 12 | Role of monocytes and macrophages in experimental and human acute liver failure显示文摘Acute liver failure (ALF) is a devastating clinical syndrome characterised by progressive encephalopathy, coagulopathy, and circulatory dysfunction, which commonly leads to multiorgan failure and death. Central to the pathogenesis of ALF is activation of the immune system with mobilisation of cellular effectors and massive production of cytokines. As key components of the innate immune system, monocytes and macrophages are postulated to play a central role in the initiation, progression and resolution of ALF. ALF in humans follows a rapidly progressive clinical course that poses inherent difficulties in delineating the role of these pivotal immune cells. Therefore, a number of experimental models have been used to study the pathogenesis of ALF. Here we consider the evidence from experimental and human studies of ALF on the role of monocytes and macrophages in acute hepatic injury and the ensuing extrahepatic manifestations, including functional monocyte deactivation and multiple organ failure. | Lucia A Possamai Charalambos Gustav Antoniades Quentin M Anstee Alberto Quaglia Diego Vergani Mark Thursz Julia Wendon | 2010 | World Journal of Gastroenterology2010，16，15： | 12 |
| 13 | Relationship between vitamin D and IL-23,IL-17 and macrophage chemoattractant protein-1 as markers of fibrosis in hepatitis C virus Egyptians显示文摘AIM:To assess vitamin D in hepatitis C patients and its relationship to interleukin (IL)-23, IL-17, and macrophage chemoattractant protein-1 (MCP-1). METHODS:The study was conducted on 50 Egyptian hepatitis C virus (HCV) genotype number IV-infected patients and 25 ageand gender-matched healthy subjects. Venous blood samples were obtained. Samples were allowed to clot and sera were separated by centrifugation and stored at -20 ℃. A 25 hydroxy vitamin D assay was carried out using solid phase RIA. A 1,25 dihydroxy vitamin D assay was carried out using a commercial kit purchased from Incstar Corporation. IL-17 and -23 and MCP-1 were assayed by an enzyme immunoassay. Quantitative and qualitative polymerase chain reaction for HCV virus were done by TaqMan technology. Only HCV genotype IV-infected subjectswere included in the study. The mean ± SD were determined, a t-test for comparison of means of different parameters was used. Correlation analysis was done using Pearson's correlation. Differences among different groups were determined using the Kruskal-Wallis test. RESULTS:The mean vitamin D level in HCV patients (groupⅠ) was 15 ± 5.2 ng/mL while in control (group Ⅱ) was 39.7 ± 10.8. For active vitamin D in groupⅠas 16.6 ± 4.8 ng/mL while in group Ⅱ was 41.9 ± 7.9. IL-23 was 154 ± 97.8 in group Ⅰ and 6.7 ± 2.17 in group Ⅱ. IL-17 was 70.7 ± 72.5 in cases and 1.2 ± 0.4 in control. MCP-1 was 1582 ± 794.4 in group Ⅰand 216.1 ± 5.38 in group Ⅱ. Vitamin D deficiency affected 72% of HCV-infected patients and 0% of the control group. Vitamin D insufficiency existed in 28% of HCV-in-fected patients and 12% of the control group. One hundred percent of the cirrhotic patients and 40% of non cirrhotic HCV-infected patients had vitamin D deficiency. IL-23, IL-17, and MCP-1 were markedly increased in HCV-infected patients in comparison to controls.A significant negative correlation between vitamin D and IL-17 and-23 and MCP-1 was detected. HCV-infected males and females showed no differences with respect to viral load, vitamin D levels, IL-17, IL-23 and MCP-1. The viral load was negatively correlated with vitamin D and active vitamin D (P = 0.0001 and P = 0.001, respectively), while positively correlated with IL-23, IL-17, and MCP-1. We classified the patients according to sonar findings into four groups. Group Ⅰa with bright hepatomegaly and included 14 patients. Group Ⅰb with perihepatic fibrosis and included 11 patients. Group Ⅰc with liver cirrhosis and included 11 patients. Group Ⅰd with he patocellular carcinoma (HCC) and included 14 patients. Vitamin D and active vitamin D were shown to be lower in cirrhotic patients and much lower in patients with HCC, and this difference was highly significant (P = 0.0001). IL-17 and-23 and MCP-1 were higher in advanced liver disease) and the differences were highly significant (P = 0.0001).CONCLUSION:Whether the deficiency of vitamin D is related to HCV-induced chronic liver disease or predisposing factor for higher viral load is a matter of debate. | Noha M El Husseiny Hala M Fahmy Waleed A Mohamed Hisham H Amin | 2012 | World Journal of Hepatology2012，4，8： | 12 |
| 14 | Hesperetin derivative-12 (HDND-12) regulates macrophage polarization by modulating JAK2/STAT3 signaling pathway显示文摘Macrophages show significant heterogeneity in function and phenotype, which could shift into different populations of cells in response to exposure to various micro-environmental signals. These changes, also termed as macrophage polarization, of which play an important role in the pathogenesis of many diseases. Numerous studies have proved that Hesperidin(HDN), a traditional Chinese medicine, extracted from fruit peels of the genus citrus, play key roles in anti-inflammation, anti-tumor, anti-oxidant and so on. However, the role of HDN in macrophage polarization has never been reported. Additional, because of its poor water solubility and bioavailability. Our laboratory had synthesized many hesperidin derivatives. Among them, hesperidin derivatives-12(HDND-12) has better water solubility and bioavailability. So, we evaluated the role of HDND-12 in macrophage polarization in the present study. The results showed that the expression of Arginase-1(Arg-1), interleukin-10(IL-10), transforming growth factor β(TGF-β) were up-regulated by HDND-12, whereas the expression of inducible Nitric Oxide Synthase(iNOS) was down-regulated in LPS-and IFN-γ-treated(M1) RAW264.7 cells. Moreover, the expression of p-JAK2 and p-STAT3 were significantly decreased after stimulation with HDND-12 in M1-like macrophages. More importantly, when we taken AG490(inhibitor of JAK2/STAT3 signaling), the protein levels of iNOS were significantly reduced in AG490 stimulation group compare with control in LPS, IFN-γ and HDND-12 stimulation cells. Taken together, these findings indicated that HDND-12 could prevent polarization toward M1-like macrophages, at least in part, through modulating JAK2/STAT3 pathway. | KONG Ling-Na LIN Xiang HUANG Cheng MA Tao-Tao MENG Xiao-Ming HU Chao-Jie WANG Qian-Qian LIU Yan-Hui SHI Qing-Ping LI Jun | 2019 | Chinese Journal of Natural Medicines2019，17，2： | 12 |
| 15 | Role of Toll-like receptors in Helicobacter pylori infection and immunity显示文摘The gram-negative bacterium Helicobacter pylori(H. pylori) infects the stomachs of approximately half of the world's population. Although infection induces an immune response that contributes to chronic gastric inflammation, the response is not sufficient to eliminate the bacterium. H. pylori infection causes peptic ulcers, gastric cancer and mucosa-associated lymphoid tissue lymphoma. Disease outcome is linked to the severity of the host inflammatory response. Gastric epithelial cells represent the first line of innate immune defence against H. pylori, and respond to infection by initiating numerous cell signalling cascades, resulting in cytokine induction and the subsequent recruitment of inflamma-tory cells to the gastric mucosa. Pathogen recognition receptors of the toll-like receptor(TLR) family mediate many of these cell signalling events. This review dis-cusses recent findings on the role of various TLRs in the recognition of H. pylori in distinct cell types, describes the TLRs responsible for the recognition of individual H. pylori components and outlines the influence of innate immune activation on the subsequent development of the adaptive immune response. The mechanistic iden-tification of host mediators of H. pylori-induced patho-genesis has the potential to reveal drug targets and opportunities for therapeutic intervention or prevention of H. pylori-associated disease by means of vaccines or immunomodulatory therapy. | Sinéad M Smith | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，3： | 11 |
| 16 | Adipocyte-derived microvesicles from obese mice induce M1 macrophage phenotype through secreted miR-155显示文摘The pro-inflammatory profile of M1 macrophage accumulation in adipose tissue is a central event leading to the metabolic complications of obesity.However,the mechanisms by which M1 macrophages are enriched in adipose tissue during weight gain remain incompletely understood.Here,we investigated the effects of adipocyte-derived microvesicles(ADM)on modulating macrophage phenotype in mice and explored the involved molecular signalling pathways.We found that,compared with ADM from lean mice(SD ADM),ADM from obese mice(HFD ADM)significantly enhanced M1 marker expression.The quantitative RTPCR assay demonstrated that miR-155 was upregulated in both HFD ADM and HFD ADM-treated macrophages.By depleting miR-155 expression in HFD ADM and increasing miR-155 level in SD ADM,we further illustrated that miR-155 in ADM-induced M1 macrophage polarization.Functionally,in contrast to SD ADM,HFD ADM significantly decreased the protein level of SOCS1,a proven miR-155 target,leading to activation of STAT1,and suppression of STAT6 signalling;these effects were reversed by silencing miR-155 in HFD ADM.Furthermore,the supernatant of bone marrow-derived macrophages pre-stimulated with miR-155-bearing ADM interfered with insulin signalling and insulin-induced glucose uptake in adipocytes.Collectively,these results provide the first evidence that M1 macrophage polarization can be mediated by miR-155-bearing ADM,which reciprocally regulates insulin signalling and glucose uptake in adipocytes.Our study reveals a novel mechanism through which obesity induces an imbalance in the M1-to-M2 macrophage ratio in adipose tissue,thus causing chronic inflammation and local insulin resistance. | Yaqin Zhang Hongliang Mei Xiaoai Chang Fang Chen Yunxia Zhu Xiao Han | 2016 | Journal of Molecular Cell Biology2016，8，6： | 11 |
| 17 | Anti-inflammation Effects of Sinomenine on Macrophages through Suppressing Activated TLR4/NF-kB Signaling Pathway显示文摘Sinomenine(SN)has been used in the clinical treatment of systemic lupus erythematosus and rheumatoid arthritis for many years.Studies showed that SN held protective effects such as anti-inflammation,scavenging free radicals and suppressing immune response in many autoimmune diseases.The purpose of the present study is to explore the mechanism of anti-inflammation of SN on lipopolysaccharide(LPS)-induced macrophages activation and investigate whether the TLR4/NF-κB signaling pathway participated in.Macrophages isolated from mouse peritoneal cavity were stimulated by 1 pg/mL LPS for 24 h.And then the cells were treated with various concentrations of SN,TLR4 inhibitor respectively for additional 48 h.Drug toxicity was detected by MTT assay and Transwell experiment was used to assess chemotaxis.Furthermore,TLR4 and MyD88 mRNA levels were detected by real-time PCR.Western blotting was used to examine TLR4,MyD88 and phosphorylated IκB protein expression in macrophages.Immunofluorescence assay was applied to observe p65 NF-κB protein expression in macrophage nucleus.We extracted macrophages with high purity and activity from the abdominal cavity of mice.SN remarkably inhibited the chemotaxis and secretion function of LPS-stimulated macrophages.It also down-regulated both the protein levels of inflammatory cytokines(TNF-α,IL-β and IL-6)and the RNA and protein levels of the key factors(TLR4,MyD88,p-IkB)in TLR4 pathway.The expression of p65 NF-κB protein in nuclei was down-regulated,which was correlated with a similar decrease in p-IκB protein level.In conclusion,SN can inhibit the LPS induced immune responses in macrophages by blocking the activated TLR4/NF-κB signaling pathway.These results may provide a therapeutic approach to regulate inflammatory responses. | Meng-you ZENG Qiao-yun TONG | 2020 | Current Medical Science2020，40，1： | 11 |
| 18 | Role of macrophages in peripheral nerve injury and repair显示文摘Resident and inflammatory macrophages are essential effectors of the innate immune system. These cells provide innate immune defenses and regulate tissue and organ homeostasis. In addition to their roles in diseases such as cancer, obesity and osteoarthritis, they play vital roles in tissue repair and disease rehabilitation. Macrophages and other inflammatory cells are recruited to tissue injury sites where they promote changes in the microenvironment. Among the inflammatory cell types, only macrophages have both pro-inflammatory (Ml) and anti-inflammatory (M2) actions, and M2 macrophages have four subtypes. The co-action of Ml and M2 subtypes can create a favorable microenvironment, releasing cytokines for damaged tissue repair. In this review, we discuss the activation of macrophages and their roles in severe peripheral nerve injury. We also describe the therapeutic potential of macrophages in nerve tissue engineering treatment and highlight approaches for enhancing M2 cell-mediated nerve repair and regeneration. | Ping Liu Jiang Peng Gong-Hai Han Xiao Ding Shuai Wei Gang Gao Kun Huang Feng Chang Yu Wang | 2019 | Neural Regeneration Research2019，14，8： | 11 |
| 19 | IL-25 stimulates M2 macrophage polarization and thereby promotes mitochondrial respiratory capacity and lipolysis in adipose tissues against obesity显示文摘Obesity and associated metabolic diseases are characterized by a chronic low-grade inflammatory state with the infiltration of many inflammatory cells,especially macrophages.Immune molecules,including some cytokines,have a close relationship with metabolism.Interleukin(IL)-25 is a member of the IL-17 cytokine family that can regulate macrophages and alleviate some metabolic dysfunction;however,its role and mechanisms in lipid metabolism remain to be extensively clarified.Human serum and liver biopsy specimens,high-fat diet-induced obesity mice and DB/DB(Lepr−/−)animal models were used to examine IL-25 expression in obesity and nonalcoholic fatty liver diseases(NAFLD).To observe the role of IL-25 in lipid metabolism,model mice were administered with IL-25 or adoptively transferred with IL-25-educated macrophages in vivo,whereas bone marrow-derived macrophages,the macrophage cell line RAW264.7 and adipocytes differentiated from 3T3-L1 were used in vitro.IL-25 was decreased in NAFLD patients and obese mice.In addition,IL-25 reduced body weight gain and lipid accumulation,enhanced lipid uptake by macrophages and increased the expression of lipolysis andβ-oxidation enzymes via alternatively activating macrophages.IL-25 also promoted lipolysis and suppressed lipogenesis in adipocytes co-cultured with the IL-25-educated macrophages.Furthermore,IL-25 improved the mitochondrial respiratory capacity and oxygen consumption rate of macrophages and produced more NAD+/NADH and ATP.In conclusion,IL-25 can stimulate M2 macrophage polarization and thereby promote lipolysis and mitochondrial respiratory capacity,highlighting the potential for IL-25 to be used as a therapeutic agent against obesity and associated metabolic syndromes. | Juan Feng Lingyi Li Zhiying Ou Qiao Li Baoyong Gong Zhenxian Zhao Weiwei Qi Ti Zhou Jun Zhong Weibin Cai Xia Yang Aiping Zhao Guoquan Gao Zhonghan Yang | 2018 | Cellular & Molecular Immunology2018，15，5： | 10 |
| 20 | Anti-inflammatory activity of curcumin-loaded tetrahedral framework nucleic acids on acute gouty arthritis显示文摘Gouty arthritis is a very familiar inflammatory arthritis.Controlling inflammation is the key to preventing gouty arthritis.However,colchicine,the most highly represented drug used in clinical practice,has strict contraindications owing to some severe side effects.Curcumin(Cur),a natural anti-inflammatory drug,has demonstrated good safety and efficacy.However,the rapid degradation,poor aqueous solubility,and low bioavailability of Cur limit its therapeutic effect.To strengthen the effectiveness and bioavailability of Cur.Cur loaded tetrahedral framework nucleic acids(Cur-TFNAs)were synthesized to deliver Cur.Compared with free Cur,Cur-TFNAs exhibit a preferable drug stability,good biocompatibility(CCK-8 assay),ease of uptake(immunofluorescence),and higher tissue utilization(in vivo biodistribution).Most importantly,Cur-TFNAs present better anti-inflammatory effect than free Cur both in vivo and in vitro experiments through the determination of inflammation-related cytokines expression.Therefore,we believe that Cur-TFNAs have great prospects for the prevention of gout and similar inflammatory diseases. | Mei Zhang Xiaolin Zhang Taoran Tian Qi Zhang Yuting Wen Junyao Zhu Dexuan Xiao Weitong Cui Yunfeng Lin | 2022 | Bioactive Materials2022，7，2： | 10 |
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