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Sofie Struyf - One of the best experts on this subject based on the ideXlab platform.

  • the cc chemokines ccl8 ccl13 and ccl20 are local inflammatory biomarkers of hla b27 associated uveitis
    Acta Ophthalmologica, 2019
    Co-Authors: Ahmed Abu M Elasrar, Nele Berghmans, Saleh A Alobeidan, Priscilla W Gikandi, Ghislain Opdenakker, Jo Van Damme, Sofie Struyf
    Abstract:

    Purpose To determine the concentrations of the CC chemokines CCL2, CCL7, CCL8, CCL11, CCL13, CCL20, CCL24 and CCL26 in aqueous humour (AH) samples from patients with specific uveitic entities. Methods Aqueous humour samples from patients with active uveitis associated with Behcet's disease (BD) (n = 13), sarcoidosis (n = 8), HLA-B27-related inflammation (n = 12), Vogt-Koyanagi-Harada (VKH) disease (n = 12) and control patients (n = 9) were assayed with the use of a multiplex assay. Results When considering all uveitis patients as one group, all chemokine levels except CCL2 were significantly increased compared to controls. CCL8, CCL13 and CCL20 were the most strongly upregulated, 48-fold, 118-fold and 173-fold, respectively, above control AH levels. CCL8 and CCL13 levels were significantly higher in HLA-B27-associated uveitis than in sarcoidosis and VKH disease. CCL20 levels were significantly higher in HLA-B27-associated uveitis than in BD, sarcoidosis and VKH disease. In addition, CCL20 levels were significantly higher in BD than in VKH disease. In HLA-B27-associated uveitis, CCL8, CCL13 and CCL20 were upregulated 111-fold, 255-fold and 465-fold, respectively, compared with controls. CCL8, CCL13 and CCL20 levels were significantly higher in nongranulomatous uveitis (BD and HLA-B27-associated uveitis) than in granulomatous uveitis (sarcoidosis and VKH disease). Conclusion Immune responses mediated by CCL8, CCL13 and CCL20 appear to be more potent in nongranulomatous uveitis, particularly in HLA-B27-associated uveitis.

  • synergistic up regulation of mcp 2 ccl8 activity is counteracted by chemokine cleavage limiting its inflammatory and anti tumoral effects
    European Journal of Immunology, 2009
    Co-Authors: Sofie Struyf, Massimo Locati, Paul Proost, Jo Vandercappellen, Sebastian Dempe, Becky Noyens, Sofie Nelissen, Mieke Gouwy, Christiane Dinsart
    Abstract:

    Chemokines mediate the inflammatory response by attracting various leukocyte types. MCP-2/CC chemokine ligand 8 (CCL8) was induced at only suboptimal levels in fibroblasts and endothelial cells by IL-1β or IFN-γ, unless these cytokines were combined. IFN-γ also synergized with the TLR ligands peptidoglycan (TLR2), dsRNA (TLR3) or LPS (TLR4). Under these conditions, intact MCP-2/CCL8(1–76) produced by fibroblasts was found to be processed into MCP-2/CCL8(6–75), which lacked chemotactic activity for monocytic cells. Furthermore, the capacity of MCP-2/CCL8(6–75) to increase intracellular calcium levels through CCR1, CCR2, CCR3 and CCR5 was severely reduced. However, the truncated isoform still blocked these receptors for other ligands. MCP-2/CCL8(6–75) induced internalization of CCR2, inhibited MCP-1/CCL2 and MCP-2/CCL8 ERK signaling and antagonized the chemotactic activity of several CCR2 ligands (MCP-1/CCL2, MCP-2/CCL8, MCP-3/CCL7). In contrast to MCP-3/CCL7, parvoviral delivery of MCP-2/CCL8 into B78/H1 melanoma failed to inhibit tumor growth, partially due to proteolytic cleavage into inactive MCP-2/CCL8 missing five NH2-terminal residues. However, in an alternative tumor model, using HeLa cells, MCP-2/CCL8 retarded tumor development. These data indicate that optimal induction and delivery of MCP-2/CCL8 is counteracted by converting this chemokine into a receptor antagonist, thereby losing its anti-tumoral potential.

  • chemokines in proliferative diabetic retinopathy and proliferative vitreoretinopathy
    European Cytokine Network, 2006
    Co-Authors: Sofie Struyf, Dustan Kangave, Karel Geboes
    Abstract:

    Purpose. To determine levels of the chemokines CCL1/I-309, CCL2/MCP-1, CCL3/MIP-1α, CCL4/MIP-1β, CCL7/MCP-3, CCL8/MCP-2, CXCL5/ENA-78, CXCL6/GCP-2, CXCL10/IP-10, and CXCL11/I-TAC in the vitreous humor and serum, from patients with proliferative diabetic retinopathy (PDR), proliferative vitreoretinopathy (PVR), and rhegmatogenous retinal detachment with no PVR (RD), and to investigate the expression of MCP-1, CXCL12/SDF-1, and the chemokine receptor CXCR3 in epiretinal membranes. Methods. Paired vitreous humor and serum samples were obtained from patients undergoing vitrectomy for the treatment of RD (57 specimens), PVR (32 specimens), and PDR (88 specimens). The levels of chemokines were measured by enzyme-linked immunosorbent assays. Eighteen PDR and 5 PVR membranes were studied by immunohistochemical techniques. Results. Of all the chemokines studied, only MCP-1 and IP-10 were detected in vitreous humor samples. MCP-1 levels in vitreous humor samples were significantly higher than in serum samples (p < 0.001). MCP-1 levels were significantly higher in vitreous humor samples from patients with PVR and PDR compared with RD (p = 0.0002). MCP-1 levels in vitreous humor samples from patients with active PDR were significantly higher than in inactive PDR cases (p = 0.0224). IP-10 levels in vitreous humor samples were significantly higher than in serum samples (p = 0.0035). IP-10 levels were significantly higher in vitreous humor samples from patients with PVR and PDR compared with RD (p = 0.0083). The incidence of IP-10 detection in vitreous humor samples was significantly higher in active PDR cases compared with inactive cases (p = 0.0214). There was a significant association between the incidence of IP-10 detection and increased levels of MCP-1 in vitreous humor samples from all patients, and patients with RD and PDR (p < 0.001 for all comparisons). MCP-1, and SDF-1 were localized in myofibroblasts in PVR and PDR membranes and in vascular endothelial cells in PDR membranes. CXCR3 was expressed by vascular endothelial cells in PDR membranes. Conclusion. MCP-1, IP-10 and SDF-1 may participate in pathogenesis of PVR and PDR. Myofibroblasts and vascular endothelial cells are the major cell types expressing MCP-1, SDF-1, and CXCR3 in epiretinal membranes.

  • identification of biologically active chemokine isoforms from ascitic fluid and elevated levels of ccl18 pulmonary and activation regulated chemokine in ovarian carcinoma
    Journal of Biological Chemistry, 2002
    Co-Authors: Evemie Schutyser, Sofie Struyf, Ghislain Opdenakker, Paul Proost, Genevieve Laureys, Bruno Verhasselt, Lieven Peperstraete, Ignace Van De Putte, Alessandra Saccani, Paola Allavena
    Abstract:

    Chemokines are important in leukocyte homeostasis, inflammation, angiogenesis, and metastasis. Here, the molecular diversity of chemokines present in ovarian carcinoma was studied by purifying the proteins to homogeneity from ascitic fluid. Biologically active intact CCL2 and processed CXCL8, CCL3, and CCL18 isoforms were recovered. CCL7 and CCL20 were also purified, but their levels were 10-fold lower compared with CXCL8, CCL2, and CCL3 and even 100-fold lower than the amounts of CCL18 isolated. In ascitic fluids from patients with ovarian carcinoma (n = 12), significantly higher levels of CXCL8 and CCL18 (2.0 versus 0.7 ng/ml (p = 0.01) and 120 versus 44 ng/ml (p = 0.0002), respectively) were detected compared with those in nonovarian carcinoma patients (n = 12). In contrast to CXCL8, CCL18 was not inducible in carcinoma cell lines. Immunostaining showed CCL18 expression in tumor-infiltrating cells with monocyte/macrophage morphology but not in the ovarian carcinoma cells. Our data demonstrate that biochemically heterogenous but biologically active forms of several chemokines are present at different concentrations in ovarian carcinoma ascitic fluid. This points to a delicate balance of chemokines in epithelial ovarian cancer and to a potentially major role for CXCL8 and CCL18 in this tumor.

Vito Pistoia - One of the best experts on this subject based on the ideXlab platform.

  • chemotaxis of human tonsil b lymphocytes to cc chemokine receptor ccr 1 ccr2 and ccr4 ligands is restricted to non germinal center cells
    International Immunology, 2002
    Co-Authors: Anna Corcione, Giuseppe Tortolina, Nicoletta Battilana, Franco Dallegri, Luciano Ottonello, Raffaella Bonecchi, Fabio Malavasi, Silvano Sozzani, Giuseppe Taborelli, Vito Pistoia
    Abstract:

    We have investigated the effects of nine CC chemokines, i.e. macrophage inflammatory protein (MIP)-1a/CCL3, MIP-1b/CCL4, MIP-3a/CCL20, MIP-5/CCL15, monocyte chemotactic protein (MCP)1/CCL2, MCP-2/CCL8, MCP-3/CCL7, eotaxin/CCL11 and macrophage-derived chemokine (MDC)/ CCL22 on the locomotion of human tonsil B lymphocytes and their subsets. Upon isolation, B cells were poorly responsive, but, following short-term culture, they displayed statistically significant chemotactic responses (P < 0.001) to MIP-1a, MIP-5, MCP-1, MCP-2, MCP-3 and MDC. CC chemokine receptor (CCR) 1 to CCR6 were up-regulated after culture. MIP-1b, MIP-3a and eotaxin did not stimulate B cell migration. Scattered information is available on B cell subset responses to chemokines. Therefore, we investigated the effects of MIP-1a, MIP-5, MCP1, MCP-2, MCP-3 and MDC on the in vitro locomotion of non-germinal center (GC) (CD38 ‐ ) and GC (CD38 + ) B cells. All chemokines enhanced significantly (P < 0.001) the migration of the former, but not of the latter, cells. CCR1, CCR2 and CCR4 were detected by flow cytometry on non-GC (i.e. naive and memory) B cells, whereas they were absent (CCR1 and CCR2) or poorly expressed (CCR4) on GC B cells.

  • chemotaxis of human tonsil b lymphocytes to cc chemokine receptor ccr 1 ccr2 and ccr4 ligands is restricted to non germinal center cells
    International Immunology, 2002
    Co-Authors: Anna Corcione, Giuseppe Tortolina, Nicoletta Battilana, Franco Dallegri, Luciano Ottonello, Raffaella Bonecchi, Fabio Malavasi, Silvano Sozzani, Giuseppe Taborelli, Vito Pistoia
    Abstract:

    We have investigated the effects of nine CC chemokines, i.e. macrophage inflammatory protein (MIP)-1alpha/CCL3, MIP-1beta/CCL4, MIP-3alpha/CCL20, MIP-5/CCL15, monocyte chemotactic protein (MCP)-1/CCL2, MCP-2/CCL8, MCP-3/CCL7, eotaxin/CCL11 and macrophage-derived chemokine (MDC)/CCL22 on the locomotion of human tonsil B lymphocytes and their subsets. Upon isolation, B cells were poorly responsive, but, following short-term culture, they displayed statistically significant chemotactic responses (P < 0.001) to MIP-1alpha, MIP-5, MCP-1, MCP-2, MCP-3 and MDC. CC chemokine receptor (CCR) 1 to CCR6 were up-regulated after culture. MIP-1beta, MIP-3alpha and eotaxin did not stimulate B cell migration. Scattered information is available on B cell subset responses to chemokines. Therefore, we investigated the effects of MIP-1alpha, MIP-5, MCP-1, MCP-2, MCP-3 and MDC on the in vitro locomotion of non-germinal center (GC) (CD38(-)) and GC (CD38(+)) B cells. All chemokines enhanced significantly (P < 0.001) the migration of the former, but not of the latter, cells. CCR1, CCR2 and CCR4 were detected by flow cytometry on non-GC (i.e. naive and memory) B cells, whereas they were absent (CCR1 and CCR2) or poorly expressed (CCR4) on GC B cells.

Hippokratis Kiaris - One of the best experts on this subject based on the ideXlab platform.

  • induction of the mcp chemokine cluster cascade in the periphery by cancer cell derived ccl3
    Cancer Letters, 2017
    Co-Authors: Elena Farmaki, Vimala Kaza, Athanasios G Papavassiliou, Ioulia Chatzistamou, Hippokratis Kiaris
    Abstract:

    The induction of localized pro-inflammatory niches in the periphery is instrumental in metastasis. In order to better understand how tumors engage distal sites and activate a pro-inflammatory response we utilized syngeneic breast cancers as a model and showed that soluble factors from the neoplastic epithelium activate the expression of the monocyte chemoattractive protein (MCP) chemokines of the mouse 11C cluster that include Ccl1, Ccl2, CCL7, Ccl8, Ccl11 and Ccl12. Tissues such as the lungs and the brain, that are more prone to colonization by breast cancer cells, were more sensitive to MCP cluster chemokine induction than others such as the liver. Subsequent analyses involving chemokine arrays in breast cancer cells and media followed by functional validation assays in in vitro and in vivo identified the cytokine Ccl3 as the principle mediator of the communication between the neoplastic epithelium and the peripheral tissues in terms of MCP cluster chemokine induction. Our results show that MCP chemokines are activated in peripheral tissues of breast cancer-bearing mice, by a mechanism that involves breast cancer cell-derived Ccl3. Interference with the expression of cancer cell-derived Ccl3 may find application in the management of breast cancer metastases.

Anna Corcione - One of the best experts on this subject based on the ideXlab platform.

  • chemotaxis of human tonsil b lymphocytes to cc chemokine receptor ccr 1 ccr2 and ccr4 ligands is restricted to non germinal center cells
    International Immunology, 2002
    Co-Authors: Anna Corcione, Giuseppe Tortolina, Nicoletta Battilana, Franco Dallegri, Luciano Ottonello, Raffaella Bonecchi, Fabio Malavasi, Silvano Sozzani, Giuseppe Taborelli, Vito Pistoia
    Abstract:

    We have investigated the effects of nine CC chemokines, i.e. macrophage inflammatory protein (MIP)-1a/CCL3, MIP-1b/CCL4, MIP-3a/CCL20, MIP-5/CCL15, monocyte chemotactic protein (MCP)1/CCL2, MCP-2/CCL8, MCP-3/CCL7, eotaxin/CCL11 and macrophage-derived chemokine (MDC)/ CCL22 on the locomotion of human tonsil B lymphocytes and their subsets. Upon isolation, B cells were poorly responsive, but, following short-term culture, they displayed statistically significant chemotactic responses (P < 0.001) to MIP-1a, MIP-5, MCP-1, MCP-2, MCP-3 and MDC. CC chemokine receptor (CCR) 1 to CCR6 were up-regulated after culture. MIP-1b, MIP-3a and eotaxin did not stimulate B cell migration. Scattered information is available on B cell subset responses to chemokines. Therefore, we investigated the effects of MIP-1a, MIP-5, MCP1, MCP-2, MCP-3 and MDC on the in vitro locomotion of non-germinal center (GC) (CD38 ‐ ) and GC (CD38 + ) B cells. All chemokines enhanced significantly (P < 0.001) the migration of the former, but not of the latter, cells. CCR1, CCR2 and CCR4 were detected by flow cytometry on non-GC (i.e. naive and memory) B cells, whereas they were absent (CCR1 and CCR2) or poorly expressed (CCR4) on GC B cells.

  • chemotaxis of human tonsil b lymphocytes to cc chemokine receptor ccr 1 ccr2 and ccr4 ligands is restricted to non germinal center cells
    International Immunology, 2002
    Co-Authors: Anna Corcione, Giuseppe Tortolina, Nicoletta Battilana, Franco Dallegri, Luciano Ottonello, Raffaella Bonecchi, Fabio Malavasi, Silvano Sozzani, Giuseppe Taborelli, Vito Pistoia
    Abstract:

    We have investigated the effects of nine CC chemokines, i.e. macrophage inflammatory protein (MIP)-1alpha/CCL3, MIP-1beta/CCL4, MIP-3alpha/CCL20, MIP-5/CCL15, monocyte chemotactic protein (MCP)-1/CCL2, MCP-2/CCL8, MCP-3/CCL7, eotaxin/CCL11 and macrophage-derived chemokine (MDC)/CCL22 on the locomotion of human tonsil B lymphocytes and their subsets. Upon isolation, B cells were poorly responsive, but, following short-term culture, they displayed statistically significant chemotactic responses (P < 0.001) to MIP-1alpha, MIP-5, MCP-1, MCP-2, MCP-3 and MDC. CC chemokine receptor (CCR) 1 to CCR6 were up-regulated after culture. MIP-1beta, MIP-3alpha and eotaxin did not stimulate B cell migration. Scattered information is available on B cell subset responses to chemokines. Therefore, we investigated the effects of MIP-1alpha, MIP-5, MCP-1, MCP-2, MCP-3 and MDC on the in vitro locomotion of non-germinal center (GC) (CD38(-)) and GC (CD38(+)) B cells. All chemokines enhanced significantly (P < 0.001) the migration of the former, but not of the latter, cells. CCR1, CCR2 and CCR4 were detected by flow cytometry on non-GC (i.e. naive and memory) B cells, whereas they were absent (CCR1 and CCR2) or poorly expressed (CCR4) on GC B cells.

Silvano Sozzani - One of the best experts on this subject based on the ideXlab platform.

  • signaling events involved in cytokine and chemokine production induced by secretory phospholipase a2 in human lung macrophages
    European Journal of Immunology, 2006
    Co-Authors: Francescopaolo Granata, Silvano Sozzani, Annunziata Frattini, Stefania Loffredo, Annalisa Del Prete, Gianni Marone, Massimo Triggiani
    Abstract:

    Secretory phospholipases A(2) (sPLA(2)) are enzymes released during inflammatory reactions. These molecules activate immune cells by mechanisms either related or unrelated to their enzymatic activity. We examined the signaling events activated by group IA (GIA) and group IB (GIB) sPLA(2) in human lung macrophages leading to cytokine/chemokine production. sPLA(2) induced the production of cytokines (TNF-alpha, IL-6 and IL-10) and chemokines (CCL2, CCL3, CCL4 and CXCL8), whereas no effect was observed on IL-12, CCL1, CCL5 and CCL22. sPLA(2) induced the phosphorylation of the MAPK p38 and ERK1/2, and inhibition of these kinases by SB203580 and PD98059, respectively, reduced TNF-alpha and CXCL8 release. Suppression of sPLA(2) enzymatic activity by a site-directed inhibitor influenced neither cytokine/chemokine production nor activation of MAPK, whereas alteration of sPLA(2) secondary structure suppressed both responses. GIA activated the phosphatidylinositol 3-kinase (PI3 K)/Akt system and a specific inhibitor of PI3 K (LY294002) reduced sPLA(2)-induced release of TNF-alpha and CXCL8. GIA promoted phosphorylation and degradation of IkappaB and inhibition of NF-kappaB by MG-132 and 6-amino-4-phenoxyphenylethylamino-quinazoline suppressed the production of TNF-alpha and CXCL8. These results indicate that sPLA(2) induce the production of cytokines and chemokines in human macrophages by a non-enzymatic mechanism involving the PI3 K/Akt system, the MAPK p38 and ERK1/2 and NF-kappaB.

  • chemotaxis of human tonsil b lymphocytes to cc chemokine receptor ccr 1 ccr2 and ccr4 ligands is restricted to non germinal center cells
    International Immunology, 2002
    Co-Authors: Anna Corcione, Giuseppe Tortolina, Nicoletta Battilana, Franco Dallegri, Luciano Ottonello, Raffaella Bonecchi, Fabio Malavasi, Silvano Sozzani, Giuseppe Taborelli, Vito Pistoia
    Abstract:

    We have investigated the effects of nine CC chemokines, i.e. macrophage inflammatory protein (MIP)-1a/CCL3, MIP-1b/CCL4, MIP-3a/CCL20, MIP-5/CCL15, monocyte chemotactic protein (MCP)1/CCL2, MCP-2/CCL8, MCP-3/CCL7, eotaxin/CCL11 and macrophage-derived chemokine (MDC)/ CCL22 on the locomotion of human tonsil B lymphocytes and their subsets. Upon isolation, B cells were poorly responsive, but, following short-term culture, they displayed statistically significant chemotactic responses (P < 0.001) to MIP-1a, MIP-5, MCP-1, MCP-2, MCP-3 and MDC. CC chemokine receptor (CCR) 1 to CCR6 were up-regulated after culture. MIP-1b, MIP-3a and eotaxin did not stimulate B cell migration. Scattered information is available on B cell subset responses to chemokines. Therefore, we investigated the effects of MIP-1a, MIP-5, MCP1, MCP-2, MCP-3 and MDC on the in vitro locomotion of non-germinal center (GC) (CD38 ‐ ) and GC (CD38 + ) B cells. All chemokines enhanced significantly (P < 0.001) the migration of the former, but not of the latter, cells. CCR1, CCR2 and CCR4 were detected by flow cytometry on non-GC (i.e. naive and memory) B cells, whereas they were absent (CCR1 and CCR2) or poorly expressed (CCR4) on GC B cells.

  • chemotaxis of human tonsil b lymphocytes to cc chemokine receptor ccr 1 ccr2 and ccr4 ligands is restricted to non germinal center cells
    International Immunology, 2002
    Co-Authors: Anna Corcione, Giuseppe Tortolina, Nicoletta Battilana, Franco Dallegri, Luciano Ottonello, Raffaella Bonecchi, Fabio Malavasi, Silvano Sozzani, Giuseppe Taborelli, Vito Pistoia
    Abstract:

    We have investigated the effects of nine CC chemokines, i.e. macrophage inflammatory protein (MIP)-1alpha/CCL3, MIP-1beta/CCL4, MIP-3alpha/CCL20, MIP-5/CCL15, monocyte chemotactic protein (MCP)-1/CCL2, MCP-2/CCL8, MCP-3/CCL7, eotaxin/CCL11 and macrophage-derived chemokine (MDC)/CCL22 on the locomotion of human tonsil B lymphocytes and their subsets. Upon isolation, B cells were poorly responsive, but, following short-term culture, they displayed statistically significant chemotactic responses (P < 0.001) to MIP-1alpha, MIP-5, MCP-1, MCP-2, MCP-3 and MDC. CC chemokine receptor (CCR) 1 to CCR6 were up-regulated after culture. MIP-1beta, MIP-3alpha and eotaxin did not stimulate B cell migration. Scattered information is available on B cell subset responses to chemokines. Therefore, we investigated the effects of MIP-1alpha, MIP-5, MCP-1, MCP-2, MCP-3 and MDC on the in vitro locomotion of non-germinal center (GC) (CD38(-)) and GC (CD38(+)) B cells. All chemokines enhanced significantly (P < 0.001) the migration of the former, but not of the latter, cells. CCR1, CCR2 and CCR4 were detected by flow cytometry on non-GC (i.e. naive and memory) B cells, whereas they were absent (CCR1 and CCR2) or poorly expressed (CCR4) on GC B cells.