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Tocris ccr5 antagonist dapta

Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the <t>CCR5</t> selective antagonist <t>DAPTA</t> (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Ccr5 Antagonist Dapta, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ccr5 antagonist dapta - by Bioz Stars, 2026-10

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1) Product Images from "Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice."

Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.

Journal: Life sciences

doi: 10.1016/j.lfs.2022.120302

Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the CCR5 selective antagonist DAPTA (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Figure Legend Snippet: Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the CCR5 selective antagonist DAPTA (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Techniques Used: Saline

Fig. 2. Determination by flow cytometry of CCR5 surface expression on CD3+, CD4+ and CD8+ T-cell subsets coming from peripheral blood collected from naïve mice. Histograms of the left-hand side depict representative examples of the fluorescence distribution (mean fluorescence intensity, MFI) detected in the APC channel (CCR5-APC) in cells coming from one sample showing the fluo rescence for the FMO sample (without CCR5 staining) and its CCR5-stained counterpart obtained in CD3+ (A), CD4+ (B) and CD8+ (C) cells. The graphs of the right-hand side show percentages of cells expressing CCR5 on CD3+ (A), CD4+ (B) and CD8+ (C). Dots correspond to individual values ob tained in each sample and red lines represent the calculated mean and the corresponding S.E. (n = 9). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Figure Legend Snippet: Fig. 2. Determination by flow cytometry of CCR5 surface expression on CD3+, CD4+ and CD8+ T-cell subsets coming from peripheral blood collected from naïve mice. Histograms of the left-hand side depict representative examples of the fluorescence distribution (mean fluorescence intensity, MFI) detected in the APC channel (CCR5-APC) in cells coming from one sample showing the fluo rescence for the FMO sample (without CCR5 staining) and its CCR5-stained counterpart obtained in CD3+ (A), CD4+ (B) and CD8+ (C) cells. The graphs of the right-hand side show percentages of cells expressing CCR5 on CD3+ (A), CD4+ (B) and CD8+ (C). Dots correspond to individual values ob tained in each sample and red lines represent the calculated mean and the corresponding S.E. (n = 9). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Techniques Used: Flow Cytometry, Expressing, Fluorescence, Staining

Fig. 9. Graphic explanation of the mechanisms proposed to be involved in the switch from analgesia to hyperalgesia when systemic doses of CCL4 are increased from pg/kg to ng/kg. The administration of 100 ng/kg of CCL4 leads to CCR5 activation and the subsequent release of IL-16 from circulating CD8+ T-cells. The activation by IL-16 of CD4 receptors expressed in CD4+ T-cells could evoke CCR5 desensitization in this lymphocyte subset, thus impeding the release of met-enk responsible on the analgesia evoked by lower doses of CCL4 [3]. Besides, the blood increase of hypernociceptive mediators, such as CCL2, CXCL1 and IL-1α [5] provokes a hyperalgesic response.

Figure Legend Snippet: Fig. 9. Graphic explanation of the mechanisms proposed to be involved in the switch from analgesia to hyperalgesia when systemic doses of CCL4 are increased from pg/kg to ng/kg. The administration of 100 ng/kg of CCL4 leads to CCR5 activation and the subsequent release of IL-16 from circulating CD8+ T-cells. The activation by IL-16 of CD4 receptors expressed in CD4+ T-cells could evoke CCR5 desensitization in this lymphocyte subset, thus impeding the release of met-enk responsible on the analgesia evoked by lower doses of CCL4 [3]. Besides, the blood increase of hypernociceptive mediators, such as CCL2, CXCL1 and IL-1α [5] provokes a hyperalgesic response.

Techniques Used: Activation Assay

Saline:

Article Title: Dual dose-related effects evoked by CCL4 on thermal nociception after gene delivery or exogenous administration in mice.
Article Snippet: As recently described, the administration of extremely low doses (pg/kg) of CCL4 (Macrophage inflammatory protein 1β, MIP-1β) can induce antinociceptive effects in mice (García-Domínguez et al., 2019b).. We describe here that hydrodynamic delivery of a plasmid containing CCL4 cDNA provokes a biphasic response consisting in an initial thermal hyperalgesic reaction for 8 days followed by analgesia at days 10–12, being both responses blocked after the administration of the CCR5 antagonist DAPTA.. Both the luminiscence evoked in liver after the administration of a plasmid containing CCL4 and luciferase cDNAs and the hepatic concentration of CCL4 measured by ELISA were maximal 4 days after plasmid administration and markedly diminished at day 10.

Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.
Article Snippet: CCL4 (100 ng/kg; ProSpec) was s.c. administered 1 h before testing dissolved in distilled water with 0.1% bovine serum albumin (Sigma). .. The CCR5 antagonist DAPTA (5 mg/kg; Tocris), the opioid receptor antagonist naloxone (3 mg/kg; Tocris) and the selective δ-opioid receptor antagonist naltrindole (1 mg/kg; Tocris) were dissolved in saline and administered s.c. 1 h, 15 min and 30 min before testing, respectively. ..

Article Title: The Chemokine CCL4 (MIP-1β) Evokes Antinociceptive Effects in Mice: a Role for CD4 + Lymphocytes and Met-Enkephalin.
Article Snippet: The CCR1 antagonist J113863 (Tocris) was dissolved in 10% dimethyl sufoxide in distilled water. .. The CCR5 antagonist DAPTA (Tocris), the non-selective opioid receptor antagonist naloxone (Tocris), the selective μ-opioid receptor antagonist cyprodime (Tocris), the selective δ-opioid receptor antagonist naltrindole (Tocris), the selective κ-opioid receptor antagonist nor-binaltorphimine (Tocris), the immunosuppressant agent cyclophosphamide (Sigma-Aldrich), the IL-1 receptor antagonist anakinra (Sigma-Aldrich), the CRF receptor antagonist α-helical CRF (9–41) (Tocris), and the anti-met-enkephalin (met-enk) antibody (ab1975, Millipore) and its corresponding control, IgG from rabbit serum (Sigma-Aldrich), were dissolved in saline. ..

Stable Transfection:

Article Title: Exchange of extracellular domains of CCR1 and CCR5 reveals confined functions in CCL5-mediated cell recruitment
Article Snippet: Birgit K. Kramp1; Remco T. A. Megens1,3; Alisina Sarabi2; Sabine Winkler2; Delia Projahn2; Christian Weber1,3,4; Rory R. Koenen1,3,*; Philipp von Hundelshausen1,4,* 1Institute for Cardiovascular Prevention, Ludwig-Maximilians-University of Munich, Munich, Germany; 2Institute for Molecular Cardiovascular Research (IMCAR), Medical Faculty, RWTH Aachen University, Aachen, Germany; 3Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands; 4DZHK (German Centre for Cardiovascular Research), partner site Munich Heart Alliance, Munich, Germany

Inhibition:

Article Title: Induction of chemokine (C‐C motif) ligand 5 by Epstein–Barr virus infection enhances tumor angiogenesis in nasopharyngeal carcinoma
Article Snippet: .. For collecting CM in chemical inhibition experiments, the PI3K inhibitor LY294002 (Selleckchem, Houston, TX, USA), the HIF‐1α inhibitor PX478 (Selleckchem), the CCR1 antagonist BX471 (Tocris, Bristol, UK), the CCR3 antagonist SB297006 (Tocris), or the CCR5 antagonist DAPTA (Tocris) was used to pretreat cells for 6 hours. ..

Injection:

Article Title: On-demand erythrocyte disposal and iron recycling requires transient macrophages in the liver
Article Snippet: Ki20227 injection : In some experiments the RBC transfer was accompanied by s.c. injection of the c-fms tyrosine kinase inhibitor Ki20227 at 50 mg/kg bodyweight (Tocris Biosciences, Bristol, UK). .. DAPTA and RS504393 injection : In some experiments the RBC transfer was accompanied by i.p injection of the Ccr2 antagonist RS504393 at 1 mg/kg bodyweight dissolved in DMSO (Tocris Biosciences, Bristol, UK) and the Ccr5 antagonist DAPTA at 2 mg/kg bodyweight (Tocris Biosciences, Bristol, UK) dissolved in sterile water. ..

Sterility:

Control:

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Journal: Life sciences

Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.

doi: 10.1016/j.lfs.2022.120302

Figure Lengend Snippet: Fig. 1. A) Thermal hyperalgesia evoked by the administration of 100 ng/kg of CCL4 (s.c.; 1 h before testing) and its prevention by the CCR5 selective antagonist DAPTA (5 mg/kg, s.c., 1 h before testing). (N = 5–6). **P < 0.01 compared with saline (SAL)-treated group, Tukey's test. On top, a diagram of the experimental design is shown. B) Mice received the i.p. administration of anti-CD3 antibody (1 μg/mouse; N = 5) or the corresponding IgG2bκ isotype (1 μg/mouse; N = 5) and 24 h later, withdrawal latencies were taken before any further treatment (BASAL). Next, mice received the acute administration of CCL4 (100 ng/kg) and 1 h later withdrawal latencies were measured again (n = 5). **P < 0.01 compared with the corresponding basal latencies, Bonferroni's correction. On top, a diagram of the experimental design is shown. C) Effect of i.p. treatment 24 h before with either anti-CD3 antibody (1 μg/mouse; N = 5) or IgG2bκ isotype (1 μg/mouse; N = 5) on the total number of circulating white blood cells, lymphocytes, mid-size cells and granulocytes. Individual data are represented as red (anti-CD3 antibody) or blue (isotype) circles and their mean and corresponding S.E. appears as a short red or blue line, respectively. **P < 0.01 compared with isotype-treated group, Bonferroni's correction. (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: The CCR5 antagonist DAPTA (5 mg/kg; Tocris), the opioid receptor antagonist naloxone (3 mg/kg; Tocris) and the selective δ-opioid receptor antagonist naltrindole (1 mg/kg; Tocris) were dissolved in saline and administered s.c. 1 h, 15 min and 30 min before testing, respectively.

Techniques: Saline

Journal: Life sciences

Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.

doi: 10.1016/j.lfs.2022.120302

Figure Lengend Snippet: Fig. 2. Determination by flow cytometry of CCR5 surface expression on CD3+, CD4+ and CD8+ T-cell subsets coming from peripheral blood collected from naïve mice. Histograms of the left-hand side depict representative examples of the fluorescence distribution (mean fluorescence intensity, MFI) detected in the APC channel (CCR5-APC) in cells coming from one sample showing the fluo rescence for the FMO sample (without CCR5 staining) and its CCR5-stained counterpart obtained in CD3+ (A), CD4+ (B) and CD8+ (C) cells. The graphs of the right-hand side show percentages of cells expressing CCR5 on CD3+ (A), CD4+ (B) and CD8+ (C). Dots correspond to individual values ob tained in each sample and red lines represent the calculated mean and the corresponding S.E. (n = 9). (For interpretation of the references to color in this figure legend, the reader is referred to the web version of this article.)

Techniques: Flow Cytometry, Expressing, Fluorescence, Staining

Journal: Life sciences

Article Title: Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice.

doi: 10.1016/j.lfs.2022.120302

Figure Lengend Snippet: Fig. 9. Graphic explanation of the mechanisms proposed to be involved in the switch from analgesia to hyperalgesia when systemic doses of CCL4 are increased from pg/kg to ng/kg. The administration of 100 ng/kg of CCL4 leads to CCR5 activation and the subsequent release of IL-16 from circulating CD8+ T-cells. The activation by IL-16 of CD4 receptors expressed in CD4+ T-cells could evoke CCR5 desensitization in this lymphocyte subset, thus impeding the release of met-enk responsible on the analgesia evoked by lower doses of CCL4 [3]. Besides, the blood increase of hypernociceptive mediators, such as CCL2, CXCL1 and IL-1α [5] provokes a hyperalgesic response.

Techniques: Activation Assay

Mean clinical scores of age- and sex-matched control mice after saline and CCR5 +/+ and CCR5 −/− mice after induction of EAE with MOG 35-55 A. Control mice group had no symptoms B. Maximal mean score was 1.8±0.2 in MOG 35-55 -immunized CCR5 −/− mice and 3.1±1.2 in MOG 35-55 -immunized CCR5 +/+ mice. Mean day of onset was the same for CCR5 +/+ (11.8±1.8) and CCR5 −/− (11.2±1.8) mice. Mean body weight (g) was compared to day 0 in each group after injection of saline or MOG 35-55 for 28 days C. At day 28, control mouse body weight had increased 3.8±2.2 g, but had decreased 3.2±3.2 g and 2.6±3.0 g in MOG35-55-immunized CCR5 +/+ and CCR5 −/− mice, respectively. Weight loss (%) was not different between MOG 35-55 -induced CCR5 +/+ (14.6±13.8) and CCR5 −/− (11.4±13.4) mice D. Values are presented as mean ± SEM. # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

Journal: Oncotarget

Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

doi: 10.18632/oncotarget.8097

Figure Lengend Snippet: Mean clinical scores of age- and sex-matched control mice after saline and CCR5 +/+ and CCR5 −/− mice after induction of EAE with MOG 35-55 A. Control mice group had no symptoms B. Maximal mean score was 1.8±0.2 in MOG 35-55 -immunized CCR5 −/− mice and 3.1±1.2 in MOG 35-55 -immunized CCR5 +/+ mice. Mean day of onset was the same for CCR5 +/+ (11.8±1.8) and CCR5 −/− (11.2±1.8) mice. Mean body weight (g) was compared to day 0 in each group after injection of saline or MOG 35-55 for 28 days C. At day 28, control mouse body weight had increased 3.8±2.2 g, but had decreased 3.2±3.2 g and 2.6±3.0 g in MOG35-55-immunized CCR5 +/+ and CCR5 −/− mice, respectively. Weight loss (%) was not different between MOG 35-55 -induced CCR5 +/+ (14.6±13.8) and CCR5 −/− (11.4±13.4) mice D. Values are presented as mean ± SEM. # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

Article Snippet: Cells were maintained in a humidified incubator at 37°C and 5% CO 2 , and were treated simultaneously with con A (4 μg/mL) and a CCR5 antagonist (D-Ala 1 -peptide T-NH 2 ; DAPTA; Bachem Bioscience Inc., King of Prussia, PA) (10 μM) dissolved in distilled water.

Techniques: Control, Saline, Injection

Cell infiltration A. and demyelination B. was greater in MOG 35-55 -immunized CCR5 +/+ mice than in MOG 35-55 -immunized CCR5 −/− mice.

Journal: Oncotarget

Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

doi: 10.18632/oncotarget.8097

Figure Lengend Snippet: Cell infiltration A. and demyelination B. was greater in MOG 35-55 -immunized CCR5 +/+ mice than in MOG 35-55 -immunized CCR5 −/− mice.

Techniques:

TNF-α protein expression in MOG 35-55 -immunized CCR5 +/+ and CCR5 −/− mouse spinal cords B. IFN-γ expression was not significantly different between MOG 35-55 -immunized CCR5 +/+ and CCR5 −/− mouse spinal cords C. MOG 35-55 injection increased IL-1β expression in CCR5 +/+ mice compared to CCR5 −/− mice D. MCP-1 expression in MOG 35-55 -immunized CCR5 +/+ mice was higher than in CCE5 −/− mice. Values are presented as mean ± SEM. * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

Journal: Oncotarget

Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

doi: 10.18632/oncotarget.8097

Figure Lengend Snippet: TNF-α protein expression in MOG 35-55 -immunized CCR5 +/+ and CCR5 −/− mouse spinal cords B. IFN-γ expression was not significantly different between MOG 35-55 -immunized CCR5 +/+ and CCR5 −/− mouse spinal cords C. MOG 35-55 injection increased IL-1β expression in CCR5 +/+ mice compared to CCR5 −/− mice D. MCP-1 expression in MOG 35-55 -immunized CCR5 +/+ mice was higher than in CCE5 −/− mice. Values are presented as mean ± SEM. * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

Techniques: Expressing, Injection, Control

CD3 + , CD4 + , CD8 + T cells did not infiltrate control mouse spinal cord tissue. MOG 35-55 -induced mouse spinal cord tissues showed infiltrating CD3 + , CD4 + , CD8 + T cells A. - C. Values are presented as mean ± SEM. ( n = 3) * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

Journal: Oncotarget

Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

doi: 10.18632/oncotarget.8097

Figure Lengend Snippet: CD3 + , CD4 + , CD8 + T cells did not infiltrate control mouse spinal cord tissue. MOG 35-55 -induced mouse spinal cord tissues showed infiltrating CD3 + , CD4 + , CD8 + T cells A. - C. Values are presented as mean ± SEM. ( n = 3) * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

Techniques: Control

CNPase (myelinating oligodendrocyte marker) A. and NG2 (oligodendrocyte precursor maker) B. expression decreased in MOG 35-55 -induced CCR5 +/+ mouse spinal cords as compared to CCR5 −/− mice spinal cord. Values are presented as mean ± SEM. ( n = 3) * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

Journal: Oncotarget

Article Title: CCR5 knockout suppresses experimental autoimmune encephalomyelitis in C57BL/6 mice

doi: 10.18632/oncotarget.8097

Figure Lengend Snippet: CNPase (myelinating oligodendrocyte marker) A. and NG2 (oligodendrocyte precursor maker) B. expression decreased in MOG 35-55 -induced CCR5 +/+ mouse spinal cords as compared to CCR5 −/− mice spinal cord. Values are presented as mean ± SEM. ( n = 3) * p < 0.05 compared to control, # p < 0.05 compared to MOG 35-55 -immunized CCR5 +/+ mice.

Techniques: Marker, Expressing, Control

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ccr5 antagonist dapta (Tocris)

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1) Product Images from "Involvement of CD4 + and CD8 + T-lymphocytes in the modulation of nociceptive processing evoked by CCL4 in mice."

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Saline:

Stable Transfection:

Inhibition:

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Sterility:

Control:

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