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1.
Braz. dent. j ; 32(3): 32-43, May-June 2021. tab, graf
Article in English | LILACS, BBO | ID: biblio-1345508

ABSTRACT

Abstract The aim of this study was to evaluate the M1 and M2 macrophage modulation after stimuli with different materials used during endodontic treatment. In bone marrow-derived macrophage cell culture, from males C57BL/6 wild-type (WT) mice, gene expression analysis of markers to M1 and M2 macrophages was performed by qRT-PCR (Cxcl10, CxCL9, iNOS, Arg1, Chil3, Retnla and MRC1) and cytokine quantification by Luminex® (GM-CSF, IL-10, IL-6, IL-1β and TNF-α) after exposure to the five endodontic sealers: AH Plus, Sealapex Xpress, Endosequence BC Sealer, BioRoot RCS and a calcium hydroxide-based paste. For normal values, ANOVA test was used, followed by Tukey post-test. For non-normal values, the Kruskall-Wallis test was used. BioRootTM RCS and EndoSequence BC SealerTM stimulated the highest expression of markers for M1 macrophages, while calcium hydroxide-based paste stimulated the lowest expression of these gene markers. For M2 protein markers, BioRootTM RCS presented the highest stimulation while calcium hydroxide-based paste also presented the lowest stimulation. It was concluded that all the evaluated filling materials increased the genetic expression of pro- and anti-inflammatory markers: TNF-α and IL-10 respectively. The others proinflammatory mediators showed differences against the filling materials. However, this process did not induce the inflammatory response polarization, resulting in a hybrid macrophage.


Resumo O objetivo deste estudo foi avaliar a modulação dos macrófagos M1 e M2 após estímulos com diferentes materiais utilizados durante o tratamento endodôntico. Em cultura de células de macrófagos derivados da medula óssea de camundongos machos C57BL/6 wild-type (WT), após a exposição à cinco cimentos endodônticos: AH Plus, Sealapex Xpress, Endosequence BC Sealer, BioRoot RCS e pasta à base de hidróxido de cálcio foi realizada a análise da expressão gênica dos marcadores para macrófagos M1 e M2 por qRT-PCR (Cxcl10, CxCL9, iNOS, Arg1, Chil3, Retnla e MRC1) e quantificação de citocinas por Luminex® (GM -CSF, IL-10, IL-6, IL-1β e TNF-α). Para valores normais, foi utilizado o teste ANOVA, seguido do pós-teste de Tukey. Para valores não normais, foi utilizado o teste de Kruskall-Wallis. BioRootTM RCS e EndoSequence BC SealerTM estimularam maior expressão de marcadores para macrófagos M1, enquanto a pasta à base de hidróxido de cálcio estimulou expressão mais baixa desses marcadores gênicos. Para o marcador de proteínas para M2, BioRootTM RCS apresentou a maior estimulação, enquanto a pasta à base de hidróxido de cálcio também apresentou menor estimulação. Concluiu-se que os materiais obturadores avaliados aumentaram a expressão genética de marcadores pró- e anti-inflamatórios: TNF-α e IL-10 respectivamente. Os demais marcadores pró inflamatórios mostraram diferenças em relação aos materiais obturadores. No entanto, esse processo não induziu a polarização da resposta inflamatória, resultando em um macrófago híbrido.


Subject(s)
Animals , Male , Rabbits , Root Canal Filling Materials , Phenotype , Materials Testing , Epoxy Resins , Macrophages , Mice, Inbred C57BL
2.
Braz. dent. j ; 32(1): 48-52, Jan.-Feb. 2021. graf
Article in English | LILACS, BBO | ID: biblio-1180718

ABSTRACT

Abstract This study evaluated the cytotoxicity of Sealapex Xpress and Real Seal XT and their effect on macrophage activation. J774.1 macrophages were incubated with Sealapex Xpress and Seal Real XT (0.1, 1.0, and 10 mg/mL) for 24 and 48 h. Cell viability was assessed by the MTT assay and macrophage activation was measured by pro- and anti-inflammatory cytokine production using ELISA. Data were analyzed using one-way ANOVA and Tukey's post-test (a=0.05). Cell viability was not affected with 0.1 or 1.0 mg/mL of extracts of Sealapex Xpress and Real Seal XT at 24 and 48 h (p>0.05), but was significantly lower when cells were exposed to 10 mg/mL of both sealers (p<0.05). Sealapex Xpress inhibited the production of TNF-a, whereas Real Seal XT induced TNF-a secretion at 24 h (p<0.05). IL-6 production was induced by Real Seal XT, but not by Sealapex Xpress (p<0.05). Real Seal XT and Sealapex Xpress induced the secretion of anti-inflammatory IL-10. IL-4 was not detected in any group. In conclusion, both sealers had low toxicity but differentially activated macrophages. Macrophage activation by Sealapex Xpress was characterized by inhibition of TNF-a and induction of IL-10, whereas Real Seal XT induced IL-6 solely.


Resumo O objetivo deste estudo foi avaliar in vitro a citotoxicidade dos cimentos endodônticos Sealapex Xpress e Real Seal XT pelo ensaio de MTT e a ativação de macrófagos J774.1. Os cimentos endodônticos Sealapex Xpress e Real Seal XT foram pesados e os extratos foram obtidos a partir da diluição em meio de cultura DMEM por 48 horas (10mg/mL, 1mg/m, e 0,1 mg/mL). A viabilidade celular foi avaliada pelo ensaio MTT e a produção de citocinas (TNF-a, IL-6 e IL-10) foi investigada pelo ensaio imunoenzimático (ELISA) em células de linhagem (macrofagos J774.1). Os dados obtidos foram analisados utilizando-se análise de variância de uma via e pós-teste de Tukey (a=0,05). A viabilidade celular após 24 ou 48 horas não foi afetada nas concentrações de 0,1 ou 1 mg/mL dos dois cimentos estudados (p>0,05). Por outro lado, na concentração 10 mg/mL, a viabilidade celular foi significativamente mais baixa (p <0,05). Observou-se que o Sealapex Xpress inibiu a produção de TNF-a, enquanto o Real Seal XT induziu a secreção de TNF-a às 24 h (p<0,05). A produção de IL-6 foi induzida pelo Real Seal XT, mas não pelo Sealapex Xpress (p<0,05). A secreção da citocina anti-inflamatória IL-10 foi induzida tanto pelo Real Seal XT quanto pelo Sealapex Xpress. IL-4 não foi detectada em nenhum grupo. Em conclusão, os dois cimentos obturadores apresentaram baixa toxicidade, mas ativaram os macrófagos de modo distinto. A ativação pelo Sealapex Xpress foi caracterizada pela inibição do TNF-a e indução da IL-10, enquanto o Real Seal XT induziu somente IL-6.


Subject(s)
Root Canal Filling Materials , Materials Testing , Calcium Hydroxide , Salicylates , Inflammation Mediators , Macrophages
3.
Electron J Biotechnol ; 49: 5-13, Jan. 2021. ilus, tab, graf
Article in English | LILACS | ID: biblio-1291618

ABSTRACT

BACKGROUND: Opsonization, is the molecular mechanism by which target molecules promote interactions with phagocyte cell surface receptors to remove unwanted cells by induced phagocytosis. We designed an in vitro system to demonstrate that this procedure could be driven to eliminate adipocytes, using peptides mimicking regions of the complement protein C3b to promote opsonization and enhance phagocytosis. Two cell lines were used: (1) THP-1 monocytes differentiated to macrophages, expressing the C3b opsonin receptor CR1 in charge of the removal of unwanted coated complexes; (2) 3T3-L1 fibroblasts differentiated to adipocytes, expressing AQP7, to evaluate the potential of peptides to stimulate opsonization. (3) A co-culture of the two cell lines to demonstrate that phagocytosis could be driven to cell withdrawal with high efficiency and specificity. RESULTS: An array of peptides were designed and chemically synthesized p3691 and p3931 joined bound to the CR1 receptor activating phagocytosis (p < 0.033) while p3727 joined the AQP7 protein (p < 0.001) suggesting that opsonization of adipocytes could occur. In the co-culture system p3980 and p3981 increased lipid uptake to 91.2% and 89.0%, respectively, as an indicator of potential adipocyte phagocytosis. CONCLUSIONS: This in vitro model could help understand the receptor­ligand interaction in the withdrawal of unwanted macromolecules in vivo. The adipocyte-phagocytosis discussed may help to control obesity, since peptides of C3b stimulated the CR1 receptor, promoting opsonisation and phagocytosis of lipidcontaining structures, and recognition of AQP7 in the differentiated adipocytes, favored the phagocytic activity of macrophages, robustly supported by the co-culture strategy.


Subject(s)
Phagocytosis , Complement System Proteins , Adipocytes , In Vitro Techniques , Opsonin Proteins , Coculture Techniques , Foam Cells , Macrophages , Microscopy, Fluorescence
4.
Article in English | WPRIM | ID: wpr-880865

ABSTRACT

Hyperglycemia induces chronic low-grade inflammation (inflammaging), which is a newly identified contributor to diabetes-related tissue lesions, including the inflammatory bone loss in periodontitis. It is also a secondary senescent pattern mediated by an increased burden of senescent cells and senescence-associated secretory phenotype (SASP). Macrophage is a key SASP-spreading cell and may contribute to the maintenance of SASP response in the periodontal microenvironment. Using a transgenic diabetic model (BLKS/J-Lepr


Subject(s)
Animals , Cellular Senescence , Diabetes Mellitus, Experimental , Glucose Transporter Type 1 , Inflammation , Macrophages , Mice
5.
Braz. arch. biol. technol ; 64: e21200736, 2021. graf
Article in English | LILACS | ID: biblio-1345489

ABSTRACT

Abstract The effects of fluorodeoxyglucose conjugated iron oxide magnetic nanoparticles (FDGMNP) on macrophages are presented using a yeast substrate. Iron oxide magnetic nanoparticles (MNP) were synthesized by partially reducing FeCl3, then conjugated with (3-aminopropyl) triethoxysilane (APTES) after silication with tetraethyl orthosilicate. Silanated MMP nanoparticles were combined with fluorodeoxyglucose (FDG). Fluorodeoxyglucose iron oxide magnetic nanoparticles (FDGMNP) and its unconjugated control (MNP) were added (1mL) to the cells from the murine macrophage-like, Abelson murine leukemia virus transformed cell line RAW 264.7 (American Type Culture Collection number TIB-71) cell culture wells at different concentrations from 90-3.6 μg/mL. Cells were placed on the magnet plate for 30 min before incubating at 37°C, 5% CO2 overnight. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium) assay was performed to measure cell viability. Our results demonstrate that iron based nanoparticles can be linked to macrophages (elements of the immune system that attack bacteria) without the function of the macrophages being affected, ie no detrimental effects to the macrophages were evident in these experiments. We conclude that neither FDGMNP nor MNP had a detrimental effect on macrophage function.


Subject(s)
Urologic Diseases , Fluorodeoxyglucose F18 , Magnetic Iron Oxide Nanoparticles , Pilot Projects , Macrophages
6.
Mem. Inst. Oswaldo Cruz ; 116: e200592, 2021. tab, graf
Article in English | LILACS | ID: biblio-1154883

ABSTRACT

BACKGROUND Paracoccidioidomycosis (PCM) is a systemic mycosis with high prevalence in Latin America that is caused by thermodimorphic fungal species of the Paracoccidioides genus. OBJECTIVES In this study, we used quantitative polymerase chain reaction (qPCR) to investigate the expression of genes related to the virulence of Paracoccidioides brasiliensis (Pb18) and P. lutzii (Pb01) strains in their mycelial (M) and yeast (Y) forms after contact with alveolar macrophages (AMJ2-C11 cell line) and fibroblasts (MRC-5 cell line). METHODS The selected genes were those coding for 43 kDa glycoprotein (gp43), enolase, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), 14-3-3 protein (30 kDa), phospholipase, and aspartyl protease. FINDINGS In the Pb18 M form, the aspartyl protease gene showed the highest expression among all genes tested, both before and after infection of host cells. In the Pb18 Y form after macrophage infection, the 14-3-3 gene showed the highest expression among all genes tested, followed by the phospholipase and gp43 genes, and their expression was 50-fold, 10-fold, and 6-fold higher, respectively, than that in the M form. After fibroblast infection with the Pb18 Y form, the 14-3-3 gene showed the highest expression, followed by the phospholipase and aspartyl protease genes, and their expression was 25-fold, 10-fold, and 10-fold higher, respectively, than that in the M form. Enolase and aspartyl protease genes were expressed upon infection of both cell lines. After macrophage infection with the Pb01 Y form, the 14-3-3 gene showed the highest expression, followed by the phospholipase and aspartyl protease genes, and their expression was 18-fold, 12.5-fold, and 6-fold higher, respectively, than that in the M form. MAIN CONCLUSIONS In conclusion, the data show that the expression of the genes analysed may be upregulated upon fungus-host interaction. Therefore, these genes may be involved in the pathogenesis of paracoccidioidomycosis.


Subject(s)
Humans , Paracoccidioides/genetics , Paracoccidioidomycosis/genetics , Virulence Factors/genetics , Fibroblasts , Macrophages , Paracoccidioides/pathogenicity , Gene Expression , Latin America
7.
Mem. Inst. Oswaldo Cruz ; 116: e200417, 2021. tab, graf
Article in English | LILACS | ID: biblio-1154880

ABSTRACT

BACKGROUND Toxoplasma gondii causes toxoplasmosis and is controlled by activated macrophages. However, infection of macrophages by tachyzoites induces TGF-β signaling (TGF-s) inhibiting nitric oxide (NO) production. NO inhibition may be a general escape mechanism of distinct T. gondii strains. OBJECTIVES To evaluate in activated macrophages the capacity of T. gondii strains of different virulence and genetics (RH, type I; ME-49, type II; VEG, type III; P-Br, recombinant) to evade the NO microbicidal defense system and determine LC3 loading to the parasitophorous vacuole. METHODS Activated peritoneal macrophages were infected with the different T. gondii strains, NO-production was evaluated by the Griess reagent, and inducible nitric oxide synthase expression, TGF-s, and LC3 localisation assayed by immunofluorescence. FINDINGS Only RH persisted in macrophages, while VEG was more resistant than P-Br and ME-49. All strains induced TGF-s, degradation of inducible nitric oxide synthase, and NO-production inhibition from 2 to 24 h of infection, but only RH sustained these alterations for 48 h. By 24 h of infection, TGF-s lowered in macrophages infected by ME-49, and P-Br, and NO-production recovered, while VEG sustained TGF-s and NO-production inhibition longer. LC3 loading to parasitophorous vacuole was strain-dependent: higher for ME-49, P-Br and VEG, lower for RH. All strains inhibited NO-production, but only RH sustained this effect probably because it persisted in macrophages due to additional evasive mechanisms as lower LC3 loading to parasitophorous vacuole. MAIN CONCLUSIONS These results support that T. gondii can escape the NO microbicidal defense system at the initial phase of the infection, but only the virulent strain sustain this evasion mechanism.


Subject(s)
Animals , Mice , Toxoplasma/physiology , Macrophages, Peritoneal/parasitology , Nitric Oxide Synthase/metabolism , Macrophages/parasitology , Nitric Oxide/biosynthesis , Toxoplasmosis, Animal/parasitology , Macrophages/metabolism
8.
Braz. j. med. biol. res ; 54(8): e11184, 2021. tab, graf
Article in English | LILACS | ID: biblio-1285676

ABSTRACT

Hypertrophic scar (HS) formation is a common complication that develops after skin injury; however, there are few effective and specific therapeutic approaches for HS. Emodin has previously been reported to inhibit mechanical stress-induced HS inflammation. Here, we investigated the molecular mechanisms underlying the inhibitory effects of emodin on HS formation. First, we conducted in vitro assays that revealed that emodin inhibited M1 and M2 polarization in rat macrophages. We subsequently established a combined rat model of tail HS and dorsal subcutaneous polyvinyl alcohol (PVA) sponge-induced wounds. Rats were treated with emodin or vehicle (DMEM). Tail scar specimens were harvested at 14, 28, and 42 days post-incision and subjected to H&E staining and Masson's trichrome staining. Histopathological analyses confirmed that emodin attenuated HS formation and fibrosis. Macrophages were separated from wound cells collected from the PVA sponge at 3 and 7 days after implantation. Flow cytometry analysis demonstrated that emodin suppressed in vivo macrophage recruitment and polarization at the wound site. Finally, we explored the molecular mechanisms of emodin in modulating macrophage polarization by evaluating the expression levels of selected effectors of the Notch and TGF-β pathways in macrophages isolated from PVA sponges. Western blot and qPCR assays showed that Notch1, Notch4, Hes1, TGF-β, and Smad3 were downregulated in response to emodin treatment. Taken together, our findings suggested that emodin attenuated HS formation and fibrosis by suppressing macrophage polarization, which is associated with the inhibition of the Notch and TGF-β pathways in macrophages.


Subject(s)
Animals , Rats , Emodin/pharmacology , Cicatrix, Hypertrophic/pathology , Cicatrix, Hypertrophic/drug therapy , Signal Transduction , Transforming Growth Factor beta , Macrophages
9.
Acta Physiologica Sinica ; (6): 244-252, 2021.
Article in Chinese | WPRIM | ID: wpr-878253

ABSTRACT

The aim of this study was to investigate the effects of polarization program on the ability of macrophages to regulate iron metabolism. M1 and M2 macrophages were propagated in vitro from porcine alveolar macrophages 3D4/2 and polarized by cytokines. The 3D4/2 macrophages were treated with 20 ng/mL interferon gamma (IFN-γ) and 10 ng/mL interleukin-4 (IL-4) combined with 10 ng/mL macrophage colony-stimulating factor (M-CSF) to induce polarization to M1 and M2, respectively. After incubation for 24 h, the expression levels of inflammatory factors and iron-metabolism genes were determined using real-time qPCR, Western bot and immunofluorescence. The M1/M2 macrophages culture media supernatant was collected and used to treat porcine intestinal epithelial cells IPEC-J2. The proliferation ability of IPEC-J2 was detected using CCK-8 assay kit. Following exogenous addition of ammonium ferric citrate (FAC) to M1/M2 macrophages, the phagocytic function of macrophages was detected using fluorescein isothiocyanate-dextran (FITC-dextran) and flow cytometry. The results showed that, compared with control, M1 macrophages had higher mRNA levels of iron storage proteins (ferritin heavy and light polypeptide, i.e. FtH and FtL), hepcidin and lipocalin-2, as well as iron content. Moreover, iron enhanced the ability of M1 macrophages to phagocytize FITC-dextran. There was no significant change in these mRNA expression levels in M2 macrophages, but the mRNA expression levels of ferroportin and transferrin receptor were up-regulated. In addition, the conditioned media supernatant from M2 macrophages promoted cell proliferation of IPEC-J2. These findings indicate that M1 macrophages tend to lock iron in the cell and reduce extracellular iron content, thereby inhibiting the proliferation of extracellular bacteria. While M2 macrophages tend to excrete iron, which contributes to the proliferation of surrounding cells and thus promotes tissue repair.


Subject(s)
Animals , Cytokines , Ferritins , Iron/metabolism , Macrophages/metabolism , Macrophages, Alveolar/metabolism , Swine
10.
Acta Physiologica Sinica ; (6): 175-180, 2021.
Article in English | WPRIM | ID: wpr-878246

ABSTRACT

The great omentum is an intraperitoneal organ and plays an important role in protecting the environment of the peritoneal cavity. Several specialized innate immune cells including B1 cells and resident macrophages are found in the omentum, which may be attributed to the unique niche and its special stromal cells. However, it is not clear how these omental innate immune cells contribute to the peritoneal immunity. This review attempts to summarize the latest research on the omental innate immunity and discuss its involvement in the immune response of the peritoneal cavity.


Subject(s)
Immunity, Innate , Macrophages , Omentum , Peritoneal Cavity , Stromal Cells
11.
Chinese Medical Journal ; (24): 699-707, 2021.
Article in English | WPRIM | ID: wpr-878065

ABSTRACT

BACKGROUND@#Autophagy of alveolar macrophages is a crucial process in ischemia/reperfusion injury-induced acute lung injury (ALI). Bone marrow-derived mesenchymal stem cells (BM-MSCs) are multipotent cells with the potential for repairing injured sites and regulating autophagy. This study was to investigate the influence of BM-MSCs on autophagy of macrophages in the oxygen-glucose deprivation/restoration (OGD/R) microenvironment and to explore the potential mechanism.@*METHODS@#We established a co-culture system of macrophages (RAW264.7) with BM-MSCs under OGD/R conditions in vitro. RAW264.7 cells were transfected with recombinant adenovirus (Ad-mCherry-GFP-LC3B) and autophagic status of RAW264.7 cells was observed under a fluorescence microscope. Autophagy-related proteins light chain 3 (LC3)-I, LC3-II, and p62 in RAW264.7 cells were detected by Western blotting. We used microarray expression analysis to identify the differently expressed genes between OGD/R treated macrophages and macrophages co-culture with BM-MSCs. We investigated the gene heme oxygenase-1 (HO-1), which is downstream of the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway.@*RESULTS@#The ratio of LC3-II/LC3-I of OGD/R treated RAW264.7 cells was increased (1.27 ± 0.20 vs. 0.44 ± 0.08, t = 6.67, P  < 0.05), while the expression of p62 was decreased (0.77 ± 0.04 vs. 0.95 ± 0.10, t = 2.90, P  < 0.05), and PI3K (0.40 ± 0.06 vs. 0.63 ± 0.10, t = 3.42, P  < 0.05) and p-Akt/Akt ratio was also decreased (0.39 ± 0.02 vs. 0.58 ± 0.03, t = 9.13, P  < 0.05). BM-MSCs reduced the LC3-II/LC3-I ratio of OGD/R treated RAW264.7 cells (0.68 ± 0.14 vs. 1.27 ± 0.20, t = 4.12, P  < 0.05), up-regulated p62 expression (1.10 ± 0.20 vs. 0.77 ± 0.04, t = 2.80, P  < 0.05), and up-regulated PI3K (0.54 ± 0.05 vs. 0.40 ± 0.06, t = 3.11, P  < 0.05) and p-Akt/Akt ratios (0.52 ± 0.05 vs. 0.39 ± 0.02, t = 9.13, P  < 0.05). A whole-genome microarray assay screened the differentially expressed gene HO-1, which is downstream of the PI3K/Akt signaling pathway, and the alteration of HO-1 mRNA and protein expression was consistent with the data on PI3K/Akt pathway.@*CONCLUSIONS@#Our results suggest the existence of the PI3K/Akt/HO-1 signaling pathway in RAW264.7 cells under OGD/R circumstances in vitro, revealing the mechanism underlying BM-MSC-mediated regulation of autophagy and enriching the understanding of potential therapeutic targets for the treatment of ALI.


Subject(s)
Apoptosis , Autophagy , Bone Marrow , Glucose , Heme Oxygenase-1/metabolism , Macrophages/metabolism , Mesenchymal Stem Cells/metabolism , Oxygen , Phosphatidylinositol 3-Kinase , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Signal Transduction
12.
Article in Chinese | WPRIM | ID: wpr-877566

ABSTRACT

OBJECTIVE@#To observe the effect of acupoint thread-embedding at "Zusanli" (ST 36) and "Fenglong" (ST 40) on the macrophage polarization of epididymis adipose tissue in obese mice, and to explore the action mechanism of acupoint thread-embedding on weight control.@*METHODS@#Among 30 male C57BL/6 mice, 10 mice were randomly selected and fed with normal diet, and the remaining 20 mice were fed with high-fat diet to establish the obesity model. Sixteen mice with successful obesity model were randomly divided into a model group and an acupoint thread-embedding group, 8 mice in each group. Eight mice were selected from mice which were fed with normal diet as the normal group. On the next day of successful modeling, acupoint thread-embedding was performed at "Zusanli" (ST 36) and "Fenglong" (ST 40) in the acupoint thread-embedding group, once every 10 days for 4 times. The body weight was recorded at 0, 8, 16, 24, 32, 40 days into intervention; the level of glucose metabolism was compared after intervention; the level of lipid metabolism and weight of epididymal adipose tissue were compared at the end of the intervention; the mRNA expression of M1 and M2 macrophage-related cytokines interleukin-10 (IL-6), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) were detected by real-time PCR; the mRNA and protein expression of M1 macrophage labeled inducible nitric oxide synthase (iNOS) and M2 macrophage labeled arginase-1 (Arg-1) were detected by real-time PCR and Western blot.@*RESULTS@#Compared with the normal group, the body weight at 0, 8, 16, 24, 32, 40 days into intervention in the model group was increased (@*CONCLUSION@#Acupoint thread-embedding at "Zusanli" (ST 36) and "Fenglong" (ST 40) may play a role in weight control by regulating the polarization of macrophages.


Subject(s)
Acupuncture Points , Adipose Tissue , Animals , Epididymis , Macrophages , Male , Mice , Mice, Inbred C57BL , Mice, Obese
13.
Rev. argent. reumatolg. (En línea) ; 31(2): 31-36, jun. 2020. ilus, tab
Article in Spanish | LILACS, BINACIS | ID: biblio-1143929

ABSTRACT

La enfermedad de Erdheim-Chester (EEC) es una histiocitosis de células no Langerhans de presentación proteiforme y escaso conocimiento. Se presenta una serie de 19 casos de 4 centros, registrados de junio de 2012 a junio de 2019. Se incluyeron aquellos pacientes con clínica, anatomía patológica e inmunohistoquímica característica de la enfermedad. Se excluyeron pacientes con hallazgos indefinidos. Resultados: al igual que en la literatura, el compromiso más frecuente fue el óseo por imagenología, la mitad de estos sintomático. Nuestra serie presenta mayor incidencia de mujeres (casi 70%). Siete pacientes presentaron nódulo mamario como forma de presentación. La mayoría recibieron dosis media de esteroides asociado a otra droga inmunosupresora. La mortalidad fue del 16%. Conclusión: comunicamos una serie de pacientes con la EEC mencionando las características más destacables. Es llamativo el número de pacientes con afectación mamaria, por lo cual proponemos téngase en cuenta en el diagnóstico diferencial de la patología tumoral mamaria.


Erdheim-Chester disease (ECD) is a non-Langerhans histiocytosis, protein manifestations at start and little known. We included 19 patients from June 2012 to June of 2019. Inclusion criteria: clinical features, histopathology and immunostaining compatible with ECD. We excluded patients with undefined features. Results: Bones were the most frequent affected, half of them were asymptomatic. Seventy per cent of the patients were women, and 7 of them developed a nodule breast as first manifestation of ECD. The patients were treated with corticosteroids associated or not with immunosuppressants. The mortality rate was 16%. Conclusion: We reported a series of patients with ECD, enhancing the most frequent features. It is striking the number of patients with breast involvement; we propose to include the Erdheim-Chester disease in differential diagnosis of breast tumor.


Subject(s)
Humans , Erdheim-Chester Disease , Giant Cells , Histiocytosis , Macrophages
14.
Autops. Case Rep ; 10(1): 2020143, Jan.-Mar. 2020. tab, ilus
Article in English | LILACS | ID: biblio-1052964

ABSTRACT

Phosphorus is a nonmetallic irritant used in various sectors like rodenticide, firecracker industries, match industries, and fertilizers. Phosphorus poisoning is responsible for deaths among children and adults. Accidental yellow phosphorus poisoning is frequently reported in children, whereas suicidal consumption is not uncommon amongst adults. Herein, we present the case of a 30-year-old female patient who ingested Ratol paste containing yellow phosphorus in an attempt to commit suicide. Her initial chief complaints were nausea, vomiting along with loose motion during hospitalization, followed by a symptomless phase with stable vitals on the 2nd day, and managed conservatively. She took discharge against the medical advice. Later on, she was readmitted in the same hospital, after two days, complaining of generalized weakness, bodily pain, drowsiness, loss of appetite, and breathing difficulties. She developed severe complications due to the intoxication and died. An autopsy was performed. The histopathological and the toxicological examination were carried out. We found characteristic features in different organs due to yellow phosphorus toxicity. We concluded the cause of death as hepatic encephalopathy and multi-organ dysfunction syndrome caused by the yellow phosphorus poisoning.


Subject(s)
Humans , Male , Middle Aged , Pneumonia, Lipid/pathology , Autopsy , Rare Diseases , Lipids , Macrophages
15.
Braz. j. med. biol. res ; 53(8): e9488, 2020. tab, graf
Article in English | LILACS, ColecionaSUS | ID: biblio-1132541

ABSTRACT

Macrophages play pivotal roles in host defense and immune homeostasis, which have two major functional polarization states, the classically activated M1 and the alternatively activated M2. Interleukin (IL)-17A is an immune modulator able to shape macrophage phenotypes. Wnt/β-catenin is a developmental signaling pathway that plays crucial roles in morphogenesis and tissue homeostasis, which has also been recently demonstrated playing roles in immune regulation. A growing amount of evidence suggests that both Wnt and IL-17A signaling are involved in macrophage polarization. However, their interaction in macrophage polarization remains elusive. The aim of present study was to explore impacts of Wnt/β-catenin on IL-17A-mediated macrophage M1/M2 polarization in murine monocyte/macrophage-like cell line RAW264.7. Results revealed that IL-17A activated Wnt/β-catenin signaling and induced macrophage M1 polarization, but inhibited M2 polarization. In contrast, the activation of Wnt/β-catenin signaling led to the inhibition of M1 macrophage polarization but the promotion of M2 polarization. Importantly, the activation of Wnt/β-catenin also showed abilities to inhibit the IL-17A-induced M1 macrophage polarization while diminishing the IL-17A-inhibited M2 polarization. Molecular analysis further uncovered that the JAK/STAT signaling pathway was involved in the interaction of Wnt/β-catenin and IL-17A in the modulation of macrophage polarization. These results suggested that the Wnt/β-catenin signaling modulated IL-17A-altered macrophage polarization in part by regulating the JAK/STAT signaling pathway. This study thus revealed a novel function of Wnt/β-catenin signaling in regulating IL-17A-altered macrophage polarization.


Subject(s)
Animals , Rats , Interleukin-17 , beta Catenin , Wnt Signaling Pathway , Macrophage Activation , Macrophages
16.
Braz. j. med. biol. res ; 53(7): e9207, 2020. tab, graf
Article in English | LILACS, ColecionaSUS | ID: biblio-1132533

ABSTRACT

The objective of this study was to investigate the relationship between PI3K/mTOR/RhoA signaling regulated cytoskeletal rearrangements and phagocytic capacity of macrophages. RAW264.7 macrophages were divided into four groups; blank control, negative control, PI3K-RNAi, and mTOR-RNAi. The cytoskeletal changes in the macrophages were observed. Furthermore, the phagocytic capacity of macrophages against Escherichia coli is reported as mean fluorescence intensity (MFI) and percent phagocytosis. Transfection yielded 82.1 and 81.5% gene-silencing efficiencies against PI3K and mTOR, respectively. The PI3K-RNAi group had lower mRNA and protein expression levels of PI3K, mTOR, and RhoA than the blank and negative control groups (Р<0.01). The mTOR-RNAi group had lower mRNA and protein levels of mTOR and RhoA than the blank and the negative control groups (Р<0.01). Macrophages in the PI3K-RNAi group exhibited stiff and inflexible morphology with short, disorganized filopodia and reduced number of stress fibers. Macrophages in the mTOR-RNAi group displayed pronounced cellular deformations with long, dense filopodia and an increased number of stress fibers. The PI3K-RNAi group exhibited lower MFI and percent phagocytosis than blank and negative control groups, whereas the mTOR-RNAi group displayed higher MFI and percent phagocytosis than the blank and negative controls (Р<0.01). Before and after transfection, the mRNA and protein levels of PI3K were both positively correlated with mTOR and RhoA (Р<0.05), but the mRNA and protein levels of mTOR were negatively correlated with those of RhoA (Р<0.05). Changes in the phagocytic capacity of macrophages were associated with cytoskeletal rearrangements and were regulated by the PI3K/mTOR/RhoA signaling pathway.


Subject(s)
Humans , Animals , Rats , Phagocytosis/physiology , Cytoskeleton/metabolism , Phosphatidylinositol 3-Kinases/metabolism , rhoA GTP-Binding Protein/metabolism , TOR Serine-Threonine Kinases/metabolism , Macrophages/metabolism , Transfection , Signal Transduction , Blotting, Western , Gene Silencing , RNA Interference , Real-Time Polymerase Chain Reaction , RAW 264.7 Cells , Genetic Vectors
17.
Article in English | WPRIM | ID: wpr-786075

ABSTRACT

Cardiovascular disease remains a leading cause of morbidity and mortality worldwide. Aspects of disease severity that are associated with heightened inflammation, such as during atherosclerosis or after myocardial infarction, are correlated with macrophage activation and macrophage polarization of the transcriptome and secretome. In this setting, non-coding RNAs (ncRNAs) may be as abundant as protein-coding genes and are increasingly recognized as significant modulators of macrophage gene expression and cytokine secretion, although the functions of most ncRNAs—and in particular, long non-coding RNAs—remain unknown. Herein, we discuss a subset of specific ncRNAs of interest in macrophages in atherosclerosis and during myocardial inflammation.


Subject(s)
Atherosclerosis , Cardiovascular Diseases , Gene Expression , Inflammation , Macrophage Activation , Macrophages , Mortality , Myocardial Infarction , RNA, Long Noncoding , RNA, Untranslated , Transcriptome
18.
Article in English | WPRIM | ID: wpr-787281

ABSTRACT

Scavenger receptors typically bind to multiple ligands on a cell surface, including endogenous and modified host-derived molecules and microbial pathogens. They promote the elimination of degraded or harmful substances such as non-self or altered-self targets through endocytosis, phagocytosis, and adhesion. Currently, scavenger receptors are subdivided into eight classes based on several variations in their sequences due to alternative splicing. Since recent studies indicate targeting scavenger receptors has been involved in cancer prognosis and carcinogenesis, we will focus on the current knowledge about the emerging role of scavenger receptor classes A to E in cancer progression.


Subject(s)
Alternative Splicing , Carcinogenesis , Endocytosis , Ligands , Macrophages , Phagocytosis , Prognosis , Receptors, Scavenger
19.
Chonnam Medical Journal ; : 12-19, 2020.
Article in English | WPRIM | ID: wpr-787279

ABSTRACT

The macrophage displays functional and phenotypic diversity, which appears, in no small part, to stem from the ability of macrophages to adapt functionally to changes in their tissue microenvironment. Here, we describe the differential activity of peritoneal macrophages with or without the presence of thioglycollate (TG), an inflammatory drug that encouraged the recruitment of macrophages, during aging. The peritoneal-resident macrophages dramatically reduced in phagocytosis and pro-inflammatory cytokines secretion with aging, whereas the functions of macrophages recruited by TG were not significantly changed with aging. These results suggest that macrophages may be changed by their environment in advanced age, and could provide possible explanations for the controversial results regarding differential changes in macrophages in other papers.


Subject(s)
Aging , Cytokines , Inflammation , Macrophages , Macrophages, Peritoneal , Phagocytosis
20.
Acta Physiologica Sinica ; (6): 227-234, 2020.
Article in Chinese | WPRIM | ID: wpr-827065

ABSTRACT

Adrenergic receptor (AR), one of the key receptors for nervous system, plays an important role in the immune microenvironment and the progression of many diseases. In recent years, the regulation of ARs and its signal on macrophages has become a research hotspot. Researchers found that ARs could exert different regulatory functions on macrophages in different microenvironments, which in turn affects occurrence and development of diseases such as tumor, heart failure, obesity, acute injury, infection and pregnancy-related diseases. This review summarizes the expression and functional regulation of ARs on macrophages, and the role of ARs in microenvironment of related diseases, which might provide new ideas for the treatments.


Subject(s)
Disease , Humans , Macrophages , Physiology , Receptors, Adrenergic , Physiology , Signal Transduction
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