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Letteratura scientifica selezionata sul tema "CCR3"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 11 marzo 2023

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Articoli di riviste sul tema "CCR3"

1

Korbecki, Jan, Klaudyna Kojder, Katarzyna Barczak, Donata Simińska, Izabela Gutowska, Dariusz Chlubek e Irena Baranowska-Bosiacka. "Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor–A Literature Review". International Journal of Molecular Sciences 21, n. 16 (6 agosto 2020): 5647. http://dx.doi.org/10.3390/ijms21165647.

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Hypoxia, i.e., oxygen deficiency condition, is one of the most important factors promoting the growth of tumors. Since its effect on the chemokine system is crucial in understanding the changes in the recruitment of cells to a tumor niche, in this review we have gathered all the available data about the impact of hypoxia on β chemokines. In the introduction, we present the chronic (continuous, non-interrupted) and cycling (intermittent, transient) hypoxia together with the mechanisms of activation of hypoxia inducible factors (HIF-1 and HIF-2) and NF-κB. Then we describe the effect of hypoxia on the expression of chemokines with the CC motif: CCL1, CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL13, CCL15, CCL16, CCL17, CCL18, CCL19, CCL20, CCL21, CCL22, CCL24, CCL25, CCL26, CCL27, CCL28 together with CC chemokine receptors: CCR1, CCR2, CCR3, CCR4, CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10. To better understand the effect of hypoxia on neoplastic processes and changes in the expression of the described proteins, we summarize the available data in a table which shows the effect of individual chemokines on angiogenesis, lymphangiogenesis, and recruitment of eosinophils, myeloid-derived suppressor cells (MDSC), regulatory T cells (Treg), and tumor-associated macrophages (TAM) to a tumor niche.

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2

Princen, Katrien, Sigrid Hatse, Kurt Vermeire, Stefano Aquaro, Erik De Clercq, Lars-Ole Gerlach, Mette Rosenkilde et al. "Inhibition of Human Immunodeficiency Virus Replication by a Dual CCR5/CXCR4 Antagonist". Journal of Virology 78, n. 23 (1 dicembre 2004): 12996–3006. http://dx.doi.org/10.1128/jvi.78.23.12996-13006.2004.

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ABSTRACT Here we report that the N-pyridinylmethyl cyclam analog AMD3451 has antiviral activity against a wide variety of R5, R5/X4, and X4 strains of human immunodeficiency virus type 1 (HIV-1) and HIV-2 (50% inhibitory concentration [IC50] ranging from 1.2 to 26.5 μM) in various T-cell lines, CCR5- or CXCR4-transfected cells, peripheral blood mononuclear cells (PBMCs), and monocytes/macrophages. AMD3451 also inhibited R5, R5/X4, and X4 HIV-1 primary clinical isolates in PBMCs (IC50, 1.8 to 7.3 μM). A PCR-based viral entry assay revealed that AMD3451 blocks R5 and X4 HIV-1 infection at the virus entry stage. AMD3451 dose-dependently inhibited the intracellular Ca2+ signaling induced by the CXCR4 ligand CXCL12 in T-lymphocytic cells and in CXCR4-transfected cells, as well as the Ca2+ flux induced by the CCR5 ligands CCL5, CCL3, and CCL4 in CCR5-transfected cells. The compound did not interfere with chemokine-induced Ca2+ signaling through CCR1, CCR2, CCR3, CCR4, CCR6, CCR9, or CXCR3 and did not induce intracellular Ca2+ signaling by itself at concentrations up to 400 μM. In freshly isolated monocytes, AMD3451 inhibited the Ca2+ flux induced by CXCL12 and CCL4 but not that induced by CCL2, CCL3, CCL5, and CCL7. The CXCL12- and CCL3-induced chemotaxis was also dose-dependently inhibited by AMD3451. Furthermore, AMD3451 inhibited CXCL12- and CCL3L1-induced endocytosis in CXCR4- and CCR5-transfected cells. AMD3451, in contrast to the specific CXCR4 antagonist AMD3100, did not inhibit but enhanced the binding of several anti-CXCR4 monoclonal antibodies (such as clone 12G5) at the cell surface, pointing to a different interaction with CXCR4. AMD3451 is the first low-molecular-weight anti-HIV agent with selective HIV coreceptor, CCR5 and CXCR4, interaction.

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3

Zvejniece, Laura, Svetlana Kozireva, Zanna Rudevica, Ainars Leonciks, Barbro Ehlin-Henriksson, Elena Kashuba e Irina Kholodnyuk. "Expression of the Chemokine Receptor CCR1 in Burkitt Lymphoma Cell Lines Is Linked to the CD10-Negative Cell Phenotype and Co-Expression of the EBV Latent Genes EBNA2, LMP1, and LMP2". International Journal of Molecular Sciences 23, n. 7 (22 marzo 2022): 3434. http://dx.doi.org/10.3390/ijms23073434.

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Chemokines and their receptors regulate the migration of immune cells and the dissemination of cancer cells. CCR1, CCR2, CCR3, and CCR5 all belong to a single protein homology cluster and respond to the same inflammatory chemokines. We previously reported that CCR1 and CCR2B are induced upon Epstein-Barr virus (EBV) infection of B cells in vitro. EBV is present in almost all cases of endemic Burkitt lymphoma (BL); however, the contribution of EBV in the pathogenesis of the disease is not fully understood. Here, we analyzed the relation of the expression of CCR1, CCR2, CCR3, and CCR5, the EBV DNA load and expression of EBV latent genes in nine EBV-carrying and four EBV-negative BL cell lines. We revealed that CCR1 is expressed at high mRNA and protein levels in two CD10-negative BL cell lines with co-expression of the EBV latent genes EBNA2, LMP1, and LMP2. Low levels of CCR2 transcripts were found in three BL cell lines. CCR3 and CCR5 transcripts were hardly detectable. Our data suggest that in vivo, CCR1 may be involved in the dissemination of BL cells and in the selection of BL cells with restricted EBV gene expression programs.

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4

Wenzl, Kerstin, Katharina Troppan, Alexander JA Deutsch, Werner Linkesch, Peter Neumeister e Christine Beham-Schmid. "Distinct Chemokine Receptor Profile In Chronic Lymphocytic Leukaemia and Richter Transformed Diffuse Large B Cell Lymphomas Compared To Germinal Center B Cells and De Novo Diffuse Large B Cell Lymphomas". Blood 122, n. 21 (15 novembre 2013): 4852. http://dx.doi.org/10.1182/blood.v122.21.4852.4852.

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Abstract Chemokine receptors are G-protein-coupled cell surface receptors, which dissociate upon activation by their ligands and cause downstream signaling. Recently, several studies have revealed the crucial contribution of chemokine receptors and their ligands in normal B-cell differentiation and development of hematopoietic malignancies. The Richter syndrome (RS) represents the clinico-pathologic transformation of chronic lymphocytic leukaemia (CLL) to an aggressive lymphoma, most commonly diffuse large B-cell lymphoma (DLBCL). Due to the lack of knowledge on the chemokine receptors in RS, we aimed to investigate their expression profile in Richter syndrome patients. Therefore, we investigated the mRNA expression levels of 18 known chemokine receptors (CCR1-CCR9, CXCR1-CXCR7, XCR1, CX3CR1) by using semi-quantitative real time PCR on seven samples of paired (CLL and transformed DLBCL) RS samples, and six samples of de novo DLBCL, additionally four CLL samples –all of them transformed into DLBCL-, and eight transformed DLBCL samples –all of them originated from CLL- were included. Four samples of peripheral B cells and four samples of germinal center B cells (GCB) served as non-neoplastic controls. 11 out of 18 chemokine receptors were differentially expressed in CLL (RL) and transformed DLBCL originated from CLL (RH) compared to GCBs. RL exhibited an at least 15-fold higher expression of CCR2, CCR4, CCR7, CXCR3, and XCR1, as well as a de novo expression of CCR3, CCR8, CXCR1, CXCR2, and CX3CR1 compared to GCB. Additionally to these chemokine receptors, CCR1 also showed significant higher expression levels comparing GCB and RH samples. Only one chemokine receptor was found to be differentially expressed in our seven paired RS samples: CCR6 showed a trend of up-regulation in CLL components. Interestingly, the transformed DLBCL originated from CLL were characterized by a significant up-regulation of six chemokine receptors (CCR3, CCR7, CXCR1, CXCR3, CXCR4, and CX3CR1) and a down-regulation of CCR5 compared to DLBCL. Our data indicate that the chemokine receptor expression profile of CLL and transformed DLBCL, originated from CLL samples, differs substantially from those of non neoplastic germinal center B cells and de novo DLBCL, suggesting other cellular origin and an impact on more aggressive clinical course of Richter syndrome patients. Hence, these multiple deregulated CC and CXC receptor might serve as useful prognostic tool to separate high malignant Richter syndrome from de novo DLBCL. Disclosures: No relevant conflicts of interest to declare.

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5

Zhang, Yi-jun, Tatjana Dragic, Yunzhen Cao, Leondios Kostrikis, Douglas S. Kwon, Dan R. Littman, Vineet N. KewalRamani e John P. Moore. "Use of Coreceptors Other Than CCR5 by Non-Syncytium-Inducing Adult and Pediatric Isolates of Human Immunodeficiency Virus Type 1 Is Rare In Vitro". Journal of Virology 72, n. 11 (1 novembre 1998): 9337–44. http://dx.doi.org/10.1128/jvi.72.11.9337-9344.1998.

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ABSTRACT We have tested a panel of pediatric and adult human immunodeficiency virus type 1 (HIV-1) primary isolates for the ability to employ the following proteins as coreceptors during viral entry: CCR1, CCR2b, CCR3, CCR4, CCR5, CCR8, CXCR4, Bonzo, BOB, GPR1, V28, US28, and APJ. Most non-syncytium-inducing isolates could utilize only CCR5. All syncytium-inducing viruses used CXCR4, some also employed V28, and one (DH123) used CCR8 and APJ as well. A longitudinal series of HIV-1 subtype B isolates from an infected infant and its mother utilized Bonzo efficiently, as well as CCR5. The maternal isolates, which were syncytium inducing, also used CXCR4, CCR8, V28, and APJ.

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6

Mazur, Grzegorz, Emilia Jaskula, Ilona Kryczek, Dorota Dlubek, Tomasz Wrobel, Aleksandra Butrym, Andrzej Lange e Kazimierz Kuliczkowski. "Gene Expression for Chemokine Receptors Influences Survival of Non-Hodgkin Lymphoma Patients". Blood 116, n. 21 (19 novembre 2010): 3103. http://dx.doi.org/10.1182/blood.v116.21.3103.3103.

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Abstract Abstract 3103 Non-Hodgkin's lymphoma (nHL) represent heterogenous group of lymphoid malignancies derived from B and T lymphocytes, NK cells or histiocytes. Most of lymphomas are B-cell origin. Lymphoma cells can migrate to other organs and their migration could be linked to chemokines and their receptors. Chemokine receptors are expressed by many cell populations, including lymphoid cells, and their main function is lymphocytes. Chemokine receptors guide lymphocytes homing, chemotaxis, adhesion and interplaying between immunologic system response cells. They are also responsible for cancer metastasis, including also dissemination of Hodgkin's and non-Hodgin's lymphomas. The purpose of the study was to determinate expression of genes coding chemokine receptors: CXCR4, CCR1, CCR2a, CCR2b, CCR3, CCR5, CCR7 and CCR8 in lymphoma lymph nodes comparing to their expression in reactive lymph nodes. We also wanted to analyze the influence of chemokine receptor gene expression on lymphoma patient survival. Methods: Chemokine receptor gene expression was evaluated in 63 lymphoma lymph nodes taken from patients (31 women and 32 men, aged 18–81 years; median age 43 years) at the moment of diagnosis. In 25 samples of reactive lymph nodes (taken from 15 women and 10 men; aged 18–59; median age 32 years) expression of chemokine genes was also studied as a control group. Gene expression of chemokine receptors CXCR4, CCR1, CCR2a, CCR2b, CCR3, CCR5, CCR7 and CCR8 was measured by reverse transcription (RT)-polymerase chain reaction method. Gene expression was estimated in arbitrary units (AU) from 0 to 3 AU points scale. PCR was conducted using primer pairs for CXCR4 (sens GAC CGC TAC CTG GCC ATC, antisens GGC AGC CAA CAG GCG AAGg A, 345 bp), CCR2a (sens GTA TCT CTC GGT GTT CTT CC, antisens TCT AGG CTC CTT CTT TGT CCT G, 271 bp), CCR2b (sens GTA TCT CTC GGT GTT CTT CC, antisens ACC AGC CGA GAC TTC CTG CT, 163 bp) CCR3 (sens TCC TTC TCT CTT CCT ATC AAT, antisens GGC AAT TTT CTG CAT CTA, 312 bp), CCR5 (sens AAT CTT CTT CAT CAT CCT CC, antisens TCT CTG TCA CCT GCA TAG C, 506 bp), CCR7 (sens CTG GTG GTG GCT CTC CTT GT, antisens GCC AGG TTG AGC AGG TAG GT, 271 bp), CCR8 (sens GGT TGG TGC TCA TTG TGG TC, antisens AGT CTA CGC TGG AGG AAC GG, 345 bp). Statistical analysis was performed using the CSS Statistica for Windows (version 7.0) software. Probability values <0.05 were considered statistically significant. Results: There was significantly higher expression of CCR1 and CCR8 gene in lymphoma lymph nodes comparing to controls (p<0.05), while CCR5 and CCR7 gene expression was significantly lower in lymphoma lymph nodes (p<0.05) comparing to reactive lymph nodes. CXCR4, CCR2a, CCR2b, CCR3 expression did not differ between lymphoma and control groups. The patients with higher expression of CCR7 gene had significantly longer survival comparing to those with lower expression (p=0.048). Expression of CCR7 was negatively correlated with IPI (p=0.036, coefficient = -0.32). Higher expression of CCR5 gene was positively correlated with Ki-67 (p=0,016, coefficient = 0.34), stage of disease (p=0.048, coefficient = 0.029) and international prognostic index score - IPI (p=0,047, coefficient = 0.298). We also found positive correlation between CCR8 gene expression and IPI (p=0.039, coefficient = 0.32). Conclusions: Lower expression of CCR7 gene is combined with longer survival of nHL patients. As there are positive correlations between CCR5 expression and Ki-67 proliferation marker and IPI as well as CCR8 and IPI in non-Hodgkin's lymphoma, those receptors can promote tumour progression. Disclosures: No relevant conflicts of interest to declare.

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7

Tiffany, H. Lee, Ghalib Alkhatib, Christophe Combadiere, Edward A. Berger e Philip M. Murphy. "CC Chemokine Receptors 1 and 3 Are Differentially Regulated by IL-5 During Maturation of Eosinophilic HL-60 Cells". Journal of Immunology 160, n. 3 (1 febbraio 1998): 1385–92. http://dx.doi.org/10.4049/jimmunol.160.3.1385.

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Abstract CC chemokine receptors 1 and 3 (CCR1 and CCR3) are expressed by eosinophils; however, factors regulating their expression and function have not previously been defined. Here we analyze chemokine receptor expression and function during eosinophil differentiation, using the eosinophilic cell line HL-60 clone 15 as a model system. RNA for CCR1, -3, -4, and -5 was not detectable in the parental cells, and the cells did not specifically bind CC chemokines. Cells treated with butyric acid acquired eosinophil characteristics; expressed mRNA for CCR1 and CCR3, but not for CCR4 or CCR5; acquired specific binding sites for macrophage-inflammatory protein-1α and eotaxin (the selective ligands for CCR1 and CCR3, respectively); and exhibited specific calcium flux and chemotaxis responses to macrophage-inflammatory protein-1α, eotaxin, and other known CCR1 and CCR3 agonists. CCR3 was expressed later and at lower levels than CCR1 and could be further induced by IL-5, whereas IL-5 had little or no effect on CCR1 expression. Consistent with the HIV-1 coreceptor activity of CCR3, HL-60 clone 15 cells induced with butyric acid and IL-5 fused with HeLa cells expressing CCR3-tropic HIV-1 envelope glycoproteins, and fusion was blocked specifically by eotaxin or an anti-CCR3 mAb. These data suggest that CCR1 and CCR3 are markers of late eosinophil differentiation that are differentially regulated by IL-5 in this model.

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8

Ortega Moreno, L., S. Fernández Tomé, M. Chaparro, A. Marin, I. Mora Gutiérrez, C. Santander, M. Baldán, J. Gisbert e D. Bernardo. "P045 Profiling of human circulating dendritic cells and monocytes subsets discriminates type and mucosal status in patients with inflammatory bowel disease". Journal of Crohn's and Colitis 14, Supplement_1 (gennaio 2020): S155—S156. http://dx.doi.org/10.1093/ecco-jcc/jjz203.174.

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Abstract Background Intestinal dendritic cells (DCs) and macrophages govern the mechanisms of immune homeostasis having a role in inflammatory bowel disease (IBD) onset. However, the profile of their circulating precursors (DC and monocytes) in IBD has not been previously described in depth. Our aim was to characterise blood DC and monocyte subsets in healthy controls (HCs) and IBD patients in order to understand their potential implication in IBD pathogenesis. Methods 18 HC and 64 IBD patients were recruited. IBD patients were categorised into Crohn’s disease (CD) and ulcerative colitis (UC), either endoscopically active (aCD and aUC) or quiescent (qCD and qUC), based on the SES-CD or the Mayo index endoscopic subscore. Blood circulating type 1 conventional DC (cDC1), type 2 conventional DC (cDC2), plasmacytoid DC (pDC), classical monocytes, non-classical monocytes and intermediate monocytes were identified by flow cytometry and characterised for the expression of 18 homing and activation markers (β7, CCR1, CCR2, CCR3, CCR5, CCR6, CCR7, CCR9, CCRL1, CD40, CD86, CD137L, CD274 (PD-L1), CLA, CXCR1, CXCR3, ICOSL and HLA-DR). Association between markers and the presence, type or activity of IBD was tested by logistic regression. Discriminant canonical analysis was also performed to classify the patients on their own endoscopy category. Results All groups (HC, aCD, qCD, aUC and qUC) were separated from the others based on the discriminant canonical analyses of the 18 markers applied over all DC and monocytes subsets (Figure 1). Specifically, CCRL1, CCR3 and CCR5 expression on cDC1, CCRL1 on non-classical monocytes and CCR9 and b7 on classical monocytes were highly associated to IBD. CCR3 displayed an odds ratio (OR) of 2.29 along with its 95% confidential interval (CI) between 1.11 and 4.75, showing a strong association with activity in CD; whereas the other markers displayed an inverse association with IBD. Hence, expression of CCRL1 on cDC1 and non-classical monocytes from aUC showed an OR (95% CI) of 0.23 (0.08–0.66) and 0.52 (0.28–0.95), respectively. In the case of qUC, CCR5 on cDC1 and β7 on classical monocytes displayed an OR (95% CI) of 0.10 (0.01–0.83) and 0.56 (0.34–0.90), respectively. CCR9 was inversely associated to qCD with an OR (95% CI) of 0.64 (0.46–0.89) in the classical monocytes subset. Indeed, the same markers (excluding β7) were also associated with IBD when all DC and monocyte subsets were considered at the same time. Conclusion Differences on the expression of migration markers CCR3, CCR5, CCR9, b7 and decoy receptor CCRL1 on circulating DC and monocyte subsets from IBD groups suggest the presence of constitutive migratory differences underlying IBD pathogenesis in CD or UC and its condition (inflamed or non-inflamed).

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Sallusto, Federica, Danielle Lenig, Charles R. Mackay e Antonio Lanzavecchia. "Flexible Programs of Chemokine Receptor Expression on Human Polarized T Helper 1 and 2 Lymphocytes". Journal of Experimental Medicine 187, n. 6 (16 marzo 1998): 875–83. http://dx.doi.org/10.1084/jem.187.6.875.

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Chemokines and their receptors are important elements for the selective attraction of various subsets of leukocytes. To better understand the selective migration of functional subsets of T cells, chemokine receptor expression was analyzed using monoclonal antibodies, RNase protection assays, and the response to distinct chemokines. Naive T cells expressed only CXC chemokine receptor (CXCR)4, whereas the majority of memory/activated T cells expressed CXCR3, and a small proportion expressed CC chemokine receptor (CCR)3 and CCR5. When polarized T cell lines were analyzed, CXCR3 was found to be expressed at high levels on T helper cell (Th)0s and Th1s and at low levels on Th2s. In contrast, CCR3 and CCR4 were found on Th2s. This was confirmed by functional responses: only Th2s responded with an increase in [Ca2+]i to the CCR3 and CCR4 agonists eotaxin and thymus and activation regulated chemokine (TARC), whereas only Th0s and Th1s responded to low concentrations of the CXCR3 agonists IFN-γ–inducible protein 10 (IP-10) and monokine induced by IFN-γ (Mig). Although CCR5 was expressed on both Th1 and Th2 lines, it was absent in several Th2 clones and its expression was markedly influenced by interleukin 2. Chemokine receptor expression and association with Th1 and Th2 phenotypes was affected by other cytokines present during polarization. Transforming growth factor β inhibited CCR3, but enhanced CCR4 and CCR7 expression, whereas interferon α inhibited CCR3 but upregulated CXCR3 and CCR1. These results demonstrate that chemokine receptors are markers of naive and polarized T cell subsets and suggest that flexible programs of chemokine receptor gene expression may control tissue-specific migration of effector T cells.

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Dragan, Paulina, Matthew Merski, Szymon Wiśniewski, Swapnil Ganesh Sanmukh e Dorota Latek. "Chemokine Receptors—Structure-Based Virtual Screening Assisted by Machine Learning". Pharmaceutics 15, n. 2 (3 febbraio 2023): 516. http://dx.doi.org/10.3390/pharmaceutics15020516.

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Chemokines modulate the immune response by regulating the migration of immune cells. They are also known to participate in such processes as cell–cell adhesion, allograft rejection, and angiogenesis. Chemokines interact with two different subfamilies of G protein-coupled receptors: conventional chemokine receptors and atypical chemokine receptors. Here, we focused on the former one which has been linked to many inflammatory diseases, including: multiple sclerosis, asthma, nephritis, and rheumatoid arthritis. Available crystal and cryo-EM structures and homology models of six chemokine receptors (CCR1 to CCR6) were described and tested in terms of their usefulness in structure-based drug design. As a result of structure-based virtual screening for CCR2 and CCR3, several new active compounds were proposed. Known inhibitors of CCR1 to CCR6, acquired from ChEMBL, were used as training sets for two machine learning algorithms in ligand-based drug design. Performance of LightGBM was compared with a sequential Keras/TensorFlow model of neural network for these diverse datasets. A combination of structure-based virtual screening with machine learning allowed to propose several active ligands for CCR2 and CCR3 with two distinct compounds predicted as CCR3 actives by all three tested methods: Glide, Keras/TensorFlow NN, and LightGBM. In addition, the performance of these three methods in the prediction of the CCR2/CCR3 receptor subtype selectivity was assessed.

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Più fonti

Tesi sul tema "CCR3"

1

Duchesnes, Cecile Emmanuelle. "Molecular characterisation of the chemokine receptor CCR3". Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407171.

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2

Brasseit, Jennifer. "Mutagenese und funktionelle Charakterisierung des humanen CCR3-Rezeptors". [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-61848.

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3

Joubert, Philippe. "Expression and function of chemokine receptors on airway smooth muscle cells". Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103385.

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Asthma is a respiratory disease that affects 2.5-3 million Canadians. This condition is characterized by a Th2-driven immune response that implicates the infiltration of eosinophils and remodelling of the airways. In the last decade, airway smooth muscle cells (ASMC) have became the subject of intense research in the field of inflammatory lung diseases including asthma. It is known that ASMC respond to a wide variety of inflammatory mediators such as cytokines and chemokines. Function of ASMC in the context of asthma has extended beyond its traditional role of a structural cell. Indeed, it is believed that they can participate in the initiation and the perpetuation of the inflammatory response that takes place in the airway of asthmatic subjects. The general aim of this work was to investigate the role of ASMC in the pathogenesis of asthma. More specifically, we studied the expression of two C-C chemokine receptors, CCR3 and CCR1 in the context of asthma.
For the first time, this work describes the expression of chemokine receptors by ASMC. We have shown that eotaxin, an important chemokine in asthma, induces migration of ASMC through the activation of CCR3. Although CCR3 expression is not regulated by Th2 cytokines in vitro, ASMC isolated from asthmatic patients expressed intrinsically higher levels of the surface receptor when compared to controls. We also describe the expression of CCR1 by ASMC, a receptor involved in airway remodelling in an animal model of asthma. We reported the expression of CCR1 mRNA in biopsies obtained from mild, moderate and severe asthmatics and showed that mild group express the highest level of CCR1. We also confirmed that ASMC express the receptor in vivo and showed that stimulation of this receptor with its ligands induces intra-cellular calcium mobilization, which confirms its functionality. Regulation of CCR1 on ASMC was also assessed using proinflammatory, Th1 and Th2 cytokines. We found that TNF-alpha and to a lesser extent, IFN-gamma, upregulated CCR1 mRNA and protein expression, while Th2 cytokines had no effect. The effect of these two cytokines was totally suppressed by either dexamethasone or mithramycin.
Collectively, our results demonstrate the expression of functional C-C chemokine receptors by ASMC. Interestingly, we have shown that CCR3 activation mediates ASMC migration and provides a new possible mechanism for the increased smooth muscle mass observed in asthmatic patients. Although the exact function of the CCR1 expressed by ASMC is unknown, our results suggest an involvement in asthma pathogenesis, possibly through airway remodelling.

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4

Fulkerson, Patricia C. "A Critical Role for Eosinophils and CCR3 Signal Transduction in Allergic Airway Disease". University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1120337075.

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5

Hablot, Julie. "Liens entre inflammations articulaire et digestive : étude expérimentale chez la souris et contribution de l’immunité mucosale". Thesis, Université de Lorraine, 2018. http://www.theses.fr/2018LORR0095/document.

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Des cellules immunitaires appartenant à l’immunité de type 3 sont localisées dans muqueuse digestive. Les micro-organismes du microbiote stimulent le système immunitaire pour le maintenir en veille face à de potentiels agents infectieux, tout en ayant une tolérance pour les micro-organismes commensaux. Des études montrent des anomalies du microbiote intestinal chez les patients arthritiques. Ceci suggère une dérégulation de l’immunité mucosale digestive dans la survenue de l’inflammation articulaire. Des cellules de l’immunité mucosale pourraient migrer vers les sites articulaires, notamment grâce à des récepteurs aux chimiokines. Le facteur RORγt, indispensable à la différenciation des cellules de l’immunité de type 3, est régulé négativement par le récepteur PPARγ. A l’aide de modèle murins, nous avons étudié l’impact de l’invalidation de PPARγ et de l’inhibition du récepteur aux chimiokines CCR3 sur les relations entre sphères digestive et articulaire. Nous avons montré que l’induction d’une colite au cours d’une arthrite au collagène modifie le microbiote intestinal, retarde l’apparition et diminue la sévérité des lésions articulaires. Nous avons démontré que les souris PPARγ-/- développent spontanément une inflammation articulaire associées à des anomalies dans la répartition des cellules immunitaires de type 3 de la muqueuse digestive. Ces souris sont dysbiotiques avec une flore enrichie notamment en entérobactéries, mais non-arthritogène. Enfin, l’inhibition de CCR3 au cours du développement d’une arthrite au collagène retarde et diminue la sévérité de la pathologie et altère la répartition des leucocytes dans les articulations et de la muqueuse digestive
Numerous type 3 immune cells (Th17 and ILC3) are physiologically located in lamina propria of the intestine. Microbial agents within the gut shape the immune system to make it efficient against threats but peaceful with commensals. Recent studies demonstrated changes in gut microbiota composition (dysbiosis) in chronic inflammatory rheumatism. These results suggest a role for mucosal immunity alteration in articular inflammation occurrence. Indeed, some type 3 immune cells once activated by microbiota, are thought to migrate to joints, involving notably chemokines receptors. Transcription factor RORγt, the master regulator of type 3 immune cells, could be negatively regulated by nuclear receptor PPARγ. Using experimental murine models, we studied the consequence of PPARγ deficiency and consequence of the chemokine receptor CCR3 inhibition on the joint-gut axis. Firstly, we demonstrated that experimental colitis induces microbiota changes, delays and reduces collagen-induced arthritis severity. Secondly, we showed that PPARγ deficient mice display spontaneous joint inflammation associated with abnormal type 3 distribution within the gut. Dysbiosis with enrichment in facultative anaerobic Enterobacteriaceae was found in these mice. Fecal microbiota transfer demonstrated this microbiota is non-arthritogenic. Finally, we demonstrated that CCR3 inhibition has profound anti-arthritic potencies associated with changes in leukocytes distribution within the joint-gut axis

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6

Kirchem, Antje. "Investigation of the signalling pathways coupled to the eotaxin receptor CCR3 in human eosinophils". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406094.

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7

Araújo, Jéssica Maria Dantas. "Participação do receptor CCR3 na migração de eosinófilos induzida por estrogênio para o útero de camundongos C57/BL6 ovariectomizados". Pós-Graduação em Ciências Fisiológicas, 2017. https://ri.ufs.br/handle/riufs/6889.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Eosinophils are commonly described as cells from innate immunity that act on parasitic infections and lung diseases. However, in recent years, new functions are being added to these cells, among them, the maintenance of reproductive homeostasis. In addition, since the 1960s, studies have shown the estrogen relationship and the selective eosinophils migration to the uterus of castrated rats. The elucidation of the mechanism for the migration of these cells appears to be based on findings showing that the CCR3 receptor and its CCL11 chemokine are expressed in the human endometrium. Objective: The objective of this study was to evaluate the CCR3 participation in the eosinophils migration to the uterus of castrated mice, induced by 17-β-estradiol (E2). Methods: C57/BL6 mice, which received subcutaneous E2 injection, were used to determine the time and dose response of E2 (times 6, 12, 24 and 48 hours and doses of 0.1, 1, 3, 10, 30, 100 and 300 μg/kg) that promotes uterine weight gain and eosinophil migration. Subsequently, using the air bubble model, we sought to standardize CCL11- induced eosinophil recruitment, and the dose of the CCR3 antagonist (SB 328437 at doses of 1, 3 and 10 mg/kg) which promotes reduction in eosinophils migration. In addition, in the same model, the effect of the uterine extract with and without the administration of E2 (at the times of 6, 12 and 24 h) on the leukocyte migration was evaluated. Finally, an investigation was carried out on the effect of SB 328437 on uterine weight and eosinophil recruitment. The eosinophil peroxidase (EPO) absorbance and histology were used to evaluate the eosinophil migration, in which the uterus was stained with orcein specific for eosinophils. Results: The results demonstrated that the dose of 100 μg/kg E2 in the 24 hour period promoted a 40% increase in uterine weight, accompanied by eosinophil migration. In the air bubble model, it was observed that CCL11 recruited eosinophils, and SB 328437 promoted a 55% reduction in migration of these cells. The extract of the uterus caused the migration of total and eosinophilic leukocytes, but there was no difference between the groups with and without the administration of E2. Corroborating the results of SB 328437 in the air bubble experiment, the evaluation of its effect on uterine weight and eosinophils recruitment demonstrated that dose of 3 mg/kg reduced both parameters (approximately 45% and 56%, respectively) when stimulated with E2. The results were analyzed using ANOVA with Tukey post-test (more than two groups), and t test (two groups). Conclusion: Based on the results, it was possible to confirm the hypothesis that the CCR3 receptor participates in the eosinophils migration to the uterus of C57/BL6 mice after E2 induction. Furthermore, it represents an important pathway to be considered in studies aimed at elucidating mechanisms in in physiological and pathological processes involving the eosinophils recruitment.
Os eosinófilos são comumente descritos como células pertencentes à imunidade inata que agem em infecções parasitárias e nas doenças pulmonares. Porém, nos últimos anos, novas funções estão sendo acrescidas a essas células, dentre as quais, de manutenção da homeostase reprodutiva. Além disso, desde a década de 60, estudos demonstraram a relação do estrogênio com a migração seletiva de eosinófilos para o útero de ratas castradas. A elucidação do mecanismo para a migração dessas células baseia-se em achados evidenciando que o receptor CCR3 e sua quimiocina CCL11 estão expressos no endométrio humano. Objetivo: Diante do exposto, o estudo objetivou avaliar a participação do CCR3 na migração de eosinófilos para o útero de camundongos castrados, induzida por 17-β-estradiol (E2). Metodologia: Camundongos C57/BL6 receberam a injeção de E2 subcutânea, objetivando determinar o tempo e a dose resposta do E2 (tempos de 6, 12, 24 e 48 horas e doses de 0,1, 1, 3, 10, 30, 100 e 300 μg/kg) que promove aumento do peso do útero e migração de eosinófilos. Posteriormente, utilizando o modelo de bolha de ar, buscou-se padronizar o recrutamento de eosinófilos induzido por CCL11, e a dose do antagonista do CCR3 (SB 328437, nas doses de 1, 3 e 10 mg/kg) que promove redução da migração de eosinófilos. Ademais, no mesmo modelo, avaliou-se o efeito do extrato do útero com e sem a administração de E2 (nos tempos de 6, 12 e 24 h), na migração de leucócitos. Por último, foi realizada uma investigação sobre o efeito do SB 328437 no peso do útero e no recrutamento de eosinófilos. Para avaliação da migração de eosinófilos foi utilizada a absorbância da Peroxidase de Eosinófilos (EPO) e a histologia, no qual, os úteros foram corados com orceína, específico para eosinófilos. Resultados: Os resultados demonstraram que a dose de 100 μg/kg de E2 no tempo de 24 horas promoveu aumento de 40% no peso do útero, acompanhado da migração de eosinófilos. No modelo de bolha de ar, observou-se que a CCL11 recrutou os eosinófilos, e o SB 328437 promoveu redução de 55% na migração dessas células. O extrato do útero provocou a migração de leucócitos totais e de eosinófilos, porém não houve diferença entre os grupos com ou sem a administração de E2. Corroborando os resultados do SB 328437 no experimento da bolha de ar, a avaliação do efeito do antagonista no peso do útero e no recrutamento de eosinófilos, demonstrou que a dose de 3 mg/kg reduziu ambos os parâmetros (aproximadamente em 45% e 56%, respectivamente) quando estimulados com E2. Os resultados foram analisados utilizando o ANOVA com pós- teste de Tukey (mais de dois grupos), e o teste t (em dois grupos). Conclusão: Perante os resultados encontrados, foi possível confirmar a hipótese de que o receptor CCR3 participa da migração de eosinófilos para o útero de camundongos C57/BL6, após indução com E2. Outrossim, representa uma importante via a ser considerada em estudos que visam a elucidação de mecanismos em processos fisiológicos e patológicos envolvendo o recrutamento de eosinófilos.
São Cristóvão, SE

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Pope, Samuel M. "Specific Role of Eotaxin-1 and Eotaxin-2 in Allergic Pulmonary Eosinophilia". Cincinnati, Ohio : University of Cincinnati, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1098472372.

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SANTUCCI, MARILINA BENEDETTA. "Ruolo della sfingosina 1-fosfato nella risposta immunitaria all’ infezione da mycobacterium tuberculosis". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2004. http://hdl.handle.net/2108/208530.

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In questa tesi è stato studiato il ruolo della sfingosina 1-fosfato (S1P) nella risposta immunitaria durante l’infezione da M. tuberculosis. La S1P è un lipide bioattivo che regola diverse funzioni biologiche cellulari. In questo contesto, è stata analizzata l’attività anti-micobatterica in cellule della linea monocito/macrofagica, THP-1 ed in una linea tumorale di cellule dell’epitelio alveolare, A549 infettate con il ceppo patogeno di M. tuberculosis H37Rv e stimolate con S1P. La crescita di M. tuberculosis è stata valutata tramite il saggio delle unità formanti colonia ed i risultati di questa analisi mostrano che la stimolazione con S1P determina un incremento dell’attività micobattericida di queste cellule. La S1P potrebbe rappresentare un componente della mucosa polmonare importante nel mantenere la sterilità al livello degli alveoli e nel regolare la risposta infiammatoria locale. In questo ambito, il passo successivo è stato quello di quantificare la S1P al livello del lavaggio broncoalveolare tramite saggio di competizione con 3HS1P. Questa analisi ha evidenziato che il contenuto di S1P al livello della mucosa polmonare di pazienti con tubercolosi polmonare attiva è più basso di quello osservato nei soggetti sani; inoltre il trattamento con S1P di cellule di lavaggio broncoalveolare (BAL) provenienti da pazienti con tubercolosi polmonare attiva, ha messo in evidenza una riduzione della crescita intracellulare dei micobatteri endogeni. Questo risultato dimostra l’efficacia dell’azione svolta dalla S1P in un sistema cellulare che riflette quello presente nel polmone profondo in corso di malattia. Al fine di analizzare se la mucosa polmonare rappresentasse un sito di accumulo dei linfociti T CD4+CCR5+ e dei linfociti TCD4+CCR3+, entrambe queste sottopopolazioni cellulari sono state studiate nel BAL e nel sangue periferico di pazienti con tubercolosi, di soggetti con malattie polmonari non correlate alla tubercolosi e di soggetti sani. Questo studio ha messo in evidenza che i linfociti T CD4+ che esprimono il recettore CCR5 o CCR3 si raccolgono 4 maggiormente nel basso tratto respiratorio rispetto al sangue periferico e che, in accordo con l’osservazione che i linfociti T CD4 del polmone di pazienti con tubercolosi polmonare sono principalmente di tipo Th1, i linfociti T CD4+CCR5+ si accumulano in maggior misura nel polmone di pazienti con tubercolosi polmonare attiva. L’obiettivo successivo di questo lavoro è stato quello di determinare se una migliore uccisione intracellulare di M. tuberculosis, dopo la stimolazione con S1P, fosse associata ad una più efficiente risposta immunitaria, vista in termini di incremento della frequenza dei linfociti T CD4+CCR5+, specifici per M. tuberculosis. A questo scopo i PBMC provenienti da pazienti con tubercolosi polmonare attiva, da soggetti con tubercolosi latente (PPD+) e da donatori sani (PPD-), sono stati infettati con M. tuberculosis e trattati con S1P. La risposta immunitaria specifica verso M. tuberculosis è stata valutata determinando la frequenza dell’espressione del CD69 su linfociti T CD4+CCR5+ del sangue periferico, dopo infezione con M. tuberculosis. I risultati di questa tesi mostrano che dopo la stimolazione con S1P dei PBMC provenienti da pazienti con tubercolosi polmonare, si assiste ad un aumento della percentuale di linfociti T specifici per M. tuberculosis senza un concomitante aumento della produzione di IFN-γ da parte delle stesse cellule. Questo risultato potrebbe essere spiegato con il fatto che nei pazienti con tubercolosi polmonare, la presenza delle cellule T regolatorie inibirebbe l’attivazione dei linfociti T specifici per M. tuberculosis, indotti dalla stimolazione con S1P, e quindi anche la produzione di IFN-γ. La mancata attivazione dei linfociti T specifici per M. tuberculosis si riflette anche in una mancata capacità di controllo della crescita intracellulare di M. tuberculosis nei PBMC di pazienti con tubercolosi polmonare dopo stimolazione con S1P; al contrario, in tre soggetti con tubercolosi latente, la stimolazione dei PBMC con S1P determina una diminuzione della crescita intracellulare di M. tuberculosis.

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Apel, Anna-Katharina [Verfasser]. "Biophysical and structural analysis of the chemokine receptors CCR2A and CCR3, leading to a 2.7 Å resolution structure of CCR2A / Anna-Katharina Apel". Ulm : Universität Ulm, 2019. http://d-nb.info/1188320963/34.

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Libri sul tema "CCR3"

1

Pass CCRN! 4^a ed. St. Louis, Mo: Elsevier, 2013.

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Pass CCRN! St.Louis, Mo: Mosby, 1996.

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R, Rogelet Keri, a cura di. Pediatric CCRN certification review. Sudbury, MA: Jones & Bartlett Learning, 2012.

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R, Rogelet Keri, a cura di. Adult CCRN certification review. Sudbury, MA: Jones and Bartlett Publishers, 2009.

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Brorsen, Ann J. Adult CCRN certification review. 2^a ed. Burlington, MA: Jones & Bartlett Learning, 2014.

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Bhat, B. V. Rajarama. Cocycles of CCR flows. Providence, R.I: American Mathematical Society, 2001.

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Horgan, Carmel Mary Teresa. Studies on Mitozolomide (CCRG 81010), a new antineoplastic agent. Birmingham: University of Aston.Department of Pharmacy, 1985.

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Gallagher, A. M. Attitudes to higher education: Report to CCRU and DENI. Belfast: Centre for Research on Higher Education, 1996.

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Centro Cultural Recoleta (Buenos Aires, Argentina), a cura di. Testa + Bedel + Benedit: 30 años del CCR. Buenos Aires: Centro Cultural Recoleta, 2010.

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LeNeveu, D. M. Analysis specifications for the CC3 vault model. Pinawa, Man: AECL Research, 1994.

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Capitoli di libri sul tema "CCR3"

1

Pease, James Edward. "Targeting CCR3". In Methods and Principles in Medicinal Chemistry, 339–57. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527631995.ch15.

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Bahl, Ash, Brian Springthorpe e Rob Riley. "Chemokine CCR3 antagonists". In New Drugs and Targets for Asthma and COPD, 153–59. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320814.

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Li, Yiwen, Deqiang Huang, Xin Xia, Zhengying Wang, Lingyu Luo e Rong Wen. "What Is the Role of CCR3 in Choroidal Neovascularization?" In Retinal Degenerative Diseases, 279–84. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0631-0_36.

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Paquet, Luc, Paolo Renzi, Nicolay Ferrari e Mark Parry-Billings. "A multitargeted antisense therapy directed at CCR3 and the common β-chain of IL-3/IL-5/GM-CSF". In New Drugs and Targets for Asthma and COPD, 297–302. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320834.

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Hütter, Gero. "CCR5". In Encyclopedia of Signaling Molecules, 828–32. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101567.

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Repeke, Carlos Eduardo, Thiago Pompermaier Garlet, Carolina Favaro Francisconi, Daiana Broll, Ana Paula Favaro Trombone e Gustavo Pompermaier Garlet. "CCL3". In Encyclopedia of Signaling Molecules, 799–804. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_579.

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Horuk, Richard. "CCR1". In Compendium of Inflammatory Diseases, 260–68. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_153.

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Hütter, Gero. "CCR5". In Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101567-1.

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Repeke, Carlos Eduardo, Thiago Pompermaier Garlet, Carolina Favaro Francisconi, Daiana Broll, Ana Paula Favaro Trombone e Gustavo Pompermaier Garlet. "CCL3". In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_579-1.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis et al. "CCL3". In Encyclopedia of Signaling Molecules, 261–65. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_579.

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Atti di convegni sul tema "CCR3"

1

Bacon, Kevin, Emma Moss, Karen Bingham, Louis-Philippe Boulet, Mark Fitzgerald, Gail Gauvreau, Paul O'Byrne et al. "LATE-BREAKING ABSTRACT: A novel role for CCR3 in promoting airways hyperreactivity; Role for CCR3-muscarinic M3 receptor heterodimers". In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa288.

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Uhm, Tae-Ki, Byung Soo Kim, Seol Kyoung Lee, Jin Hyun Kang, Do Jin Kim e Il Yup Chung. "CCR3 Transcriptional Control By Multiple, But Not A Single, Gata Elements". In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5717.

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Proboszcz, Małgorzata, Patrycja Nejman-Gryz, Magdalena Paplińska-Goryca, Katarzyna Górska, Paulina Misiukiewicz-Stępień e Rafał Krenke. "Expression of CCR3 on sputum macrophages in asthma, COPD and healthy subjects". In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4085.

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Ueki, S., G. Mahemuti, H. Kato, M. Takeda, J. Kihara, M. Tanabe, W. Ito, H. Kayaba e J. Chihara. "Retinoic Acids Induce Survival, Cytokine Production, and Expression of CCR3 on Human Eosinophils." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1359.

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Valdameri, Joana Scapinello, Anna Carolina Flumignan Bucharles, Caroline Baldasso Vieira, Thainá Mirella Macedo e Maria Luiza Lyczacovski Riesemberg. "CLASSIFICAÇÃO E CARACTERÍSTICAS HISTOLÓGICA DOS CARCINOMAS DE CÉLULAS RENAIS MAIS FREQUENTES". In I Congresso On-line Nacional de Histologia e Embriologia Humana. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/rems/3214.

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Introdução: O carcinoma de células renais (CCR), tumor frequente na população, é caracterizado pelo aumento de massa no parênquima renal, onde encontram-se as unidades funcionais do rim. Sua nova classificação, publicada em 2016 pela WHO (World Health Organization), é baseada em aspectos histológicos que variam conforme os subtipos. Objetivos: Identificar histopatologicamente os principais subtipos de carcinomas de células renais, evidenciando melhor decisão de terapia para melhor prognóstico. Material e métodos: A metodologia consistiu em uma revisão literária de artigos publicados em língua inglesa ou portuguesa, nas bases de dados “Pubmed” e "Scielo", no período entre 2018 e 2022. Foram utilizados como descritores “carcinoma real” e “histologia de carcinoma", e feito leitura dos artigos de maior relevância, considerando cronologia e local de publicação. Resultados: Por meio da análise dos artigos, foi evidenciado que o CCR está entre os tumores mais frequentes na população, sendo os subtipos mais recorrentes os carcinomas renais das células claras (CCRcc), seguidos pelos tipos papilíferos (CCRp) e cromófobos (CCRc). Sua classificação baseia-se em aspectos histológicos, e sua nomenclatura está associada ao citoplasma típico de células tumorais, bem como características estruturais e morfológicas. O CCRcc, que corresponde entre 65 e 70% dos casos, apresenta prognóstico desfavorável. Possui origem no epitélio do túbulo contorcido proximal e é caracterizado pela presença de células claras devido ao citoplasma eosinofílico rico em lipídios e glicogênio. O CCRp, de origem histológica no néfron distal e epitélio tubular, se caracteriza por um tumor imperceptível à palpação, e é dividido em dois subtipos, um com citoplasma escasso e outro com citoplasma eosinofílico. Por fim, o CCRc se origina de células intercalares dos ductos coletores, sendo menos agressivo e mais comum após 60 anos representa 5% dos CCR, possui prognóstico favorável, com baixa incidência de metástase. Existem, ainda, outros subtipos, porém são menos frequentes em relação aos expostos anteriormente. Conclusão: Diante do exposto, nota-se a importância da classificação histológica dos CCR, facilitando a compreensão da função e da composição dos tecidos lesionados, com o objetivo de realizar o prognóstico e tratamento adequado.

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Yao, Xin, Xiaoyi Yan, Xinyu Jiang, Jie Jiang, Man Jia e Mao Huang. "IL-4/13-induced up-regulation of METEORIN-LIKE (ML) in alveolar macrophages promotes epithelial CCR3 expression". In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3552.

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Krammer, Susanne, Nina Li, Zuqin Yang, Julia Koelle, Carol Immanuel Geppert, Ralf J. Rieker, Gerard Graham e Susetta Finotto. "Late Breaking Abstract - The Role of the chemokine receptor CCR3 in House Dust Mite (HDM) induced experimental asthma". In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.306.

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Dosanjh, Amrita, e Sunil M. Kurian. "Activation Of Eosinophil CCR3 Signaling And Eotaxin Using A Bioinformatics Approach To Study A Mouse Model Of Obliterative Airway Disease". In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5133.

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Moura, Maria Eduarda Gobara de, Letícia Ganem Rillo Paz Barateiro, Jacqueline Zanone e Jaqueline de Carvalho Rinaldi. "AVALIAÇÃO DA POPULAÇÃO DE MASTÓCITOS DA PRÓSTATA DORSOLATERAL DE RATOS WISTAR". In I Congresso Brasileiro de Estudos Patológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbesp/19.

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Introdução: Terapias convencionais para o câncer podem causar diversos efeitos colaterais, logo, uma alternativa são os suplementos nutricionais imunomoduladores como os simbióticos. Enquanto o probiótico Bifidobacterium animalis tem potencial antiinflamatório e protege a microbiota intestinal, o prebiótico quercetina destaca-se pela atividade antioxidante. Embora a maioria dos estudos avaliem impactos desses compostos individualmente e no sistema digestório, são escassos aqueles que os unem e investigam seus efeitos em órgãos como os reprodutores. Como a próstata, que se alterada, pode afetar a nutrição espermática e sucesso reprodutivo, também, a qualidade de vida do paciente. Objetivo: O objetivo deste trabalho foi avaliar impactos do uso B. animalis e quercetina na resposta imune, quantificando os mastócitos totais da próstata dorsolateral de ratos com câncer colorretal. Material e métodos: vinte-e-cinco ratos Wistar machos foram divididos em 5 grupos (n=5): Controle (C), com câncer colorretal (CCR), CCR e tratados com quercetina (CCRQ), CCR e tratados com probiótico (CCRP) e CCR tratados com ambos os compostos (CCRPQ). O câncer colorretal foi incitado com a administração de 1,2-dimetilhidrazina (DMH) duas vezes por semana, durante 14 dias (40 mg/kg). Os tratamentos envolvendo quercetina foram na dose de 10mg/kg diariamente e B. animalis em solução com 5x107UFC no volume adequado ao peso de cada animal. Após eutanásia, a próstata foi dissecada, pesada, fixada em methacarn e emblocada em parafina. Cortes de 5 µm de espessura foram corados com azul de toluidina, para quantificação de mastócitos com auxílio da microscopia de luz. Os dados foram submetidos à análise de variância ANOVA, sendo estatístico o p<=0,05. Resultado: Foi observado diminuição na quantidade de mastócitos totais de animais do grupo CCRPQ (média=55 mastócitos/animal) quando comparados ao CCR (média=139,75 mastócitos/animal). Análises comparativas entre todos os grupos, mostraram valor de p significativo somente entre CCR e CCRPQ (p=0,0441). Conclusão: A atividade simbiótica de B. animalis e quercetina alterou a população total de mastócitos na próstata dorsolateral em comparação aos animais induzidos com câncer. Embora estes resultados sejam promissores, são parciais, sendo que mais análises estão em andamento para compreensão dos mecanismos envolvidos

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Nanni, Bernardino P., Justin L. Bolender e Spencer D. Whittier. "Wastewater Treatment in Support of Ash Pond Closures". In ASME 2013 Power Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/power2013-98091.

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The Environmental Protection Agency (EPA) is evaluating rules that will not permit the storage of coal combustion residuals (CCRs) in surface impoundments, and require CCRs to be stored in Subtitle C or Subtitle D landfills. In addition, the EPA is evaluating more stringent effluent guidelines for water discharges which may impact NPDES permits in the future. To support these changes, the Tennessee Valley Authority (TVA) is evaluating the elimination of wet CCR handling and surface impoundments at their coal fired facilities. If CCR conveyance is converted to dry methods and the surface impoundments are closed, the other wastewater streams that utilize these impoundments as a point of discharge will also be affected. Therefore, TVA is investigating options to handle the miscellaneous wastewater streams that currently discharge to the impoundments, and meet more stringent effluent limits that may be implemented in the future. This investigation includes characterization of the existing wastewater streams, determining the effects on wastewater streams associated with future plant modifications and anticipated regulatory changes, developing methods to reduce and reuse wastewater streams to avoid discharge, and developing methods to treat the remaining wastewater streams that may be discharged in accordance with potential future effluent limits. TVA is in the forefront of addressing the pending EPA rules that may affect CCR handling and storage, and water discharges. This paper discusses and presents the process being used by TVA to address these changes, the results obtained to date, and how this may be applicable to others potentially impacted by these changes.

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Rapporti di organizzazioni sul tema "CCR3"

1

Adair, M. The CCRS Quicklook Swath Browser. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2000. http://dx.doi.org/10.4095/219632.

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2

Adair, M. The CCRS Quicklook Swath Browser. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2000. http://dx.doi.org/10.4095/219646.

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3

Cyr, I., e Th Toutin. RADARSAT-1 Stereo Advisor on CCRS Web. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2001. http://dx.doi.org/10.4095/219705.

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4

Graham, D. F., A. N. Rencz e V. H. Singhroy. GSC - CCRS Storefront Project, conclusions from selected projects. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1994. http://dx.doi.org/10.4095/193706.

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5

Vachon, P. W., A. L. Gray e K. E. Mattar. RADARSAT and ERS Repeat-Pass SAR Interferometry at CCRS. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1998. http://dx.doi.org/10.4095/219176.

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6

Boyle, J. S. Comparison of CCM3 simulations using two climatological ozone data sets. Office of Scientific and Technical Information (OSTI), febbraio 1997. http://dx.doi.org/10.2172/632787.

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7

Bentz, Dale P., Xiuping Feng, Claus-Jochen Haecker e Paul E. Stutzman. Analysis of CCRL proficiency cements 135 and 136 using CEMHYD3D. Gaithersburg, MD: National Institute of Standards and Technology, 2000. http://dx.doi.org/10.6028/nist.ir.6545.

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8

Wolfe, S. A. Permafrost science at ESS: a workshop on GSC/CCRS scientific opportunities. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2010. http://dx.doi.org/10.4095/263373.

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9

McGurrin, B. Remote Sensing Information: How and Why CCRS Developed an Online Database. Natural Resources Canada/CMSS/Information Management, 1990. http://dx.doi.org/10.4095/217657.

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10

Banks, G. N., J. K. Wong e H. Whaley. Combustion evaluation of eureka residue in the CCRL pilot-scale flame tunnel furnace. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1989. http://dx.doi.org/10.4095/304418.

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