human ril 33 Search Results


mouse ril 33  (Enzo Biochem)
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Enzo Biochem mouse ril 33
Increasing IL‐33 levels exacerbates OA in vivo . (a) protein and (b) mRNA expression of cartilage‐degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in isolated human chondrocytes from Non‐OA ( n = 20) and OA patients ( n = 20) treated with either PBS (vehicle control) or <t>rIL‐33</t> (30 ng mL −1 , 24 h). (c) MMP‐13 and (d) MMP‐3 protein level in cell media supernatants obtained from isolated human chondrocytes from Non‐OA ( n = 12) and OA patients ( n = 12) treated with either PBS (vehicle control) or rIL‐33 (30 ng mL −1 ; 24 h). (e, f) OARSI scoring of cartilage tissue, (g) synovitis scoring and (h) osteophyte maturity scoring of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). (i) von Frey pain assessment of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). (j) mRNA expression of cartilage‐degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in whole knee joints of DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). All RT‐qPCR gene expressions were normalised to the endogenous level of 18 s in respective groups. Data are expressed as mean ± S.E.M. with unpaired 2‐tailed Student’s t ‐tests ( c, d ), two‐way analysis of variance followed by the Tukey‐Kramer test ( f, g, h ), or repeated measures 2‐way ANOVA with Bonferroni’s post hoc tests was used to compare groups at each time point (i; DMM PBS vs DMM rIL‐33). n indicates the number of human specimens or mice per group. NS = non‐significant. P < 0.01, P < 0.001 or P < 0.0001 are represented as **, *** or ****, respectively.
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Increasing IL‐33 levels exacerbates OA in vivo . (a) protein and (b) mRNA expression of cartilage‐degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in isolated human chondrocytes from Non‐OA ( n = 20) and OA patients ( n = 20) treated with either PBS (vehicle control) or rIL‐33 (30 ng mL −1 , 24 h). (c) MMP‐13 and (d) MMP‐3 protein level in cell media supernatants obtained from isolated human chondrocytes from Non‐OA ( n = 12) and OA patients ( n = 12) treated with either PBS (vehicle control) or rIL‐33 (30 ng mL −1 ; 24 h). (e, f) OARSI scoring of cartilage tissue, (g) synovitis scoring and (h) osteophyte maturity scoring of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). (i) von Frey pain assessment of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). (j) mRNA expression of cartilage‐degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in whole knee joints of DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). All RT‐qPCR gene expressions were normalised to the endogenous level of 18 s in respective groups. Data are expressed as mean ± S.E.M. with unpaired 2‐tailed Student’s t ‐tests ( c, d ), two‐way analysis of variance followed by the Tukey‐Kramer test ( f, g, h ), or repeated measures 2‐way ANOVA with Bonferroni’s post hoc tests was used to compare groups at each time point (i; DMM PBS vs DMM rIL‐33). n indicates the number of human specimens or mice per group. NS = non‐significant. P < 0.01, P < 0.001 or P < 0.0001 are represented as **, *** or ****, respectively.

Journal: Clinical & Translational Immunology

Article Title: Blockade of IL‐33 signalling attenuates osteoarthritis

doi: 10.1002/cti2.1187

Figure Lengend Snippet: Increasing IL‐33 levels exacerbates OA in vivo . (a) protein and (b) mRNA expression of cartilage‐degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in isolated human chondrocytes from Non‐OA ( n = 20) and OA patients ( n = 20) treated with either PBS (vehicle control) or rIL‐33 (30 ng mL −1 , 24 h). (c) MMP‐13 and (d) MMP‐3 protein level in cell media supernatants obtained from isolated human chondrocytes from Non‐OA ( n = 12) and OA patients ( n = 12) treated with either PBS (vehicle control) or rIL‐33 (30 ng mL −1 ; 24 h). (e, f) OARSI scoring of cartilage tissue, (g) synovitis scoring and (h) osteophyte maturity scoring of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). (i) von Frey pain assessment of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). (j) mRNA expression of cartilage‐degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in whole knee joints of DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either PBS (vehicle control) or rIL‐33 (33 μg kg −1 ; daily for 12 weeks post‐surgery). All RT‐qPCR gene expressions were normalised to the endogenous level of 18 s in respective groups. Data are expressed as mean ± S.E.M. with unpaired 2‐tailed Student’s t ‐tests ( c, d ), two‐way analysis of variance followed by the Tukey‐Kramer test ( f, g, h ), or repeated measures 2‐way ANOVA with Bonferroni’s post hoc tests was used to compare groups at each time point (i; DMM PBS vs DMM rIL‐33). n indicates the number of human specimens or mice per group. NS = non‐significant. P < 0.01, P < 0.001 or P < 0.0001 are represented as **, *** or ****, respectively.

Article Snippet: For experiments which increased IL‐33 levels in vivo , mouse rIL‐33 (Enzo Life Sciences, Farmingdale) was administered intraperitoneally (i.p) on a daily basis at 33 μg kg −1 for 12 weeks post‐surgery.

Techniques: In Vivo, Expressing, Isolation, Quantitative RT-PCR

Neutralising ST2 attenuates OA. (a, b) OARSI scoring of cartilage tissue, (c) synovitis scoring and (d) osteophyte maturity scoring of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either IgG1 (vehicle control; 50 µg per mouse; daily for 12 weeks post‐surgery) or αST2 (50 µg per mouse; daily for 12 weeks post‐surgery). (e) von Frey pain assessment of sham‐ ( n = 20) or DMM‐ ( n = 20) operated WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either IgG1 (vehicle control; 50 µg per mouse; daily for 12 weeks post‐surgery) or αST2 (50 µg per mouse; daily for 12 weeks post‐surgery). (f) mRNA expression of cartilage‐degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in whole knee joints of DMM‐operated ( n = 20) treated intraperitoneally with either IgG1 (vehicle control; 50 µg per mouse; daily for 12 weeks post‐surgery) or αST2 (50 µg per mouse; daily for 12 weeks post‐surgery). (g) protein and (h) mRNA expression of cartilage degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in isolated human chondrocytes from Non‐OA ( n = 20) and OA patients ( n = 20) treated with rIL‐33 (30 ng mL −1 , 24 h) and IgG1 (vehicle control; 3 μg mL −1 , 24 h) or αST2 (3 μg mL −1 , 24 h). (i) MMP‐13 (j) MMP‐3 protein level in cell media supernatants obtained from isolated human chondrocytes from Non‐OA ( n = 12) and OA patients ( n = 12) treated with rIL‐33 (30 ng mL −1 ; 24 h) and IgG1 (vehicle control; 3 μg mL −1 , 24 h) or αST2 (3 μg mL −1 , 24 h). All RT‐qPCR gene expressions were normalised to the endogenous level of 18 s in respective groups. Data are expressed as mean ± S.E.M. with two‐way analysis of variance followed by the Tukey‐Kramer test (b, c, d) or repeated measures 2‐way ANOVA with Bonferroni’s post hoc tests was used to compare groups at each time point ( e ; DMM IgG1 control mice vs DMM αST2 mice) or with unpaired 2‐tailed Student’s t ‐tests (i, j) . n indicates the number of human specimens or mice per group. NS = non‐significant. P < 0.001 or P < 0.0001 are represented as *** or ****, respectively.

Journal: Clinical & Translational Immunology

Article Title: Blockade of IL‐33 signalling attenuates osteoarthritis

doi: 10.1002/cti2.1187

Figure Lengend Snippet: Neutralising ST2 attenuates OA. (a, b) OARSI scoring of cartilage tissue, (c) synovitis scoring and (d) osteophyte maturity scoring of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either IgG1 (vehicle control; 50 µg per mouse; daily for 12 weeks post‐surgery) or αST2 (50 µg per mouse; daily for 12 weeks post‐surgery). (e) von Frey pain assessment of sham‐ ( n = 20) or DMM‐ ( n = 20) operated WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either IgG1 (vehicle control; 50 µg per mouse; daily for 12 weeks post‐surgery) or αST2 (50 µg per mouse; daily for 12 weeks post‐surgery). (f) mRNA expression of cartilage‐degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in whole knee joints of DMM‐operated ( n = 20) treated intraperitoneally with either IgG1 (vehicle control; 50 µg per mouse; daily for 12 weeks post‐surgery) or αST2 (50 µg per mouse; daily for 12 weeks post‐surgery). (g) protein and (h) mRNA expression of cartilage degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in isolated human chondrocytes from Non‐OA ( n = 20) and OA patients ( n = 20) treated with rIL‐33 (30 ng mL −1 , 24 h) and IgG1 (vehicle control; 3 μg mL −1 , 24 h) or αST2 (3 μg mL −1 , 24 h). (i) MMP‐13 (j) MMP‐3 protein level in cell media supernatants obtained from isolated human chondrocytes from Non‐OA ( n = 12) and OA patients ( n = 12) treated with rIL‐33 (30 ng mL −1 ; 24 h) and IgG1 (vehicle control; 3 μg mL −1 , 24 h) or αST2 (3 μg mL −1 , 24 h). All RT‐qPCR gene expressions were normalised to the endogenous level of 18 s in respective groups. Data are expressed as mean ± S.E.M. with two‐way analysis of variance followed by the Tukey‐Kramer test (b, c, d) or repeated measures 2‐way ANOVA with Bonferroni’s post hoc tests was used to compare groups at each time point ( e ; DMM IgG1 control mice vs DMM αST2 mice) or with unpaired 2‐tailed Student’s t ‐tests (i, j) . n indicates the number of human specimens or mice per group. NS = non‐significant. P < 0.001 or P < 0.0001 are represented as *** or ****, respectively.

Article Snippet: For experiments which increased IL‐33 levels in vivo , mouse rIL‐33 (Enzo Life Sciences, Farmingdale) was administered intraperitoneally (i.p) on a daily basis at 33 μg kg −1 for 12 weeks post‐surgery.

Techniques: Expressing, Isolation, Quantitative RT-PCR

Neutralising IL‐33 attenuates OA. (a, b) OARSI scoring of cartilage tissue, (c) synovitis scoring and (d) osteophyte maturity scoring of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either IgG1 (vehicle control; 15 µg per mouse; daily for 12 weeks post‐surgery) or αIL‐33 (15 µg per mouse; daily for 12 weeks post‐surgery). (e) von Frey pain assessment of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either IgG1 (vehicle control; 15 µg per mouse; daily for 12 weeks post‐surgery) or αIL‐33 (15 µg per mouse; daily for 12 weeks post‐surgery). (f) mRNA expression of cartilage degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in whole knee joints of DMM‐operated ( n = 20) treated intraperitoneally with either IgG1 (vehicle control; 15 µg per mouse; daily for 12 weeks post‐surgery) or αIL‐33 (15 µg per mouse; daily for 12 weeks post‐surgery). (g) protein and (h) mRNA expression of cartilage degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in isolated human chondrocytes from Non‐OA ( n = 20) and OA patients ( n = 20) treated with rIL‐33 (30 ng mL −1 , 24 h) and IgG1 (vehicle control; 10 μg mL −1 , 24 h) or αIL‐33 (10 μg mL −1 , 24 h). (i) MMP‐13 ( j) MMP‐3 protein level in cell media supernatants obtained from isolated human chondrocytes from Non‐OA ( n = 12) and OA patients ( n = 12) treated with rIL‐33 (30 ng mL −1 ; 24 h) and IgG1 (vehicle control; 10 μg mL −1 , 24 h) or αIL‐33 (10 μg mL −1 , 24 h). All RT‐qPCR gene expressions were normalised to the endogenous level of 18 s in respective groups. Data are expressed as mean ± S.E.M. with two‐way analysis of variance followed by the Tukey‐Kramer test ( b, c, d ) or repeated measures 2‐way ANOVA with Bonferroni’s post hoc tests was used to compare groups at each time point ( e ; DMM IgG1 control mice vs DMM αIL‐33 mice) or with unpaired 2‐tailed Student’s t ‐tests ( i, j ). n indicates the number of human specimens or mice per group. NS = non‐significant. P < 0.0001 is represented as ****.

Journal: Clinical & Translational Immunology

Article Title: Blockade of IL‐33 signalling attenuates osteoarthritis

doi: 10.1002/cti2.1187

Figure Lengend Snippet: Neutralising IL‐33 attenuates OA. (a, b) OARSI scoring of cartilage tissue, (c) synovitis scoring and (d) osteophyte maturity scoring of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either IgG1 (vehicle control; 15 µg per mouse; daily for 12 weeks post‐surgery) or αIL‐33 (15 µg per mouse; daily for 12 weeks post‐surgery). (e) von Frey pain assessment of sham‐operated ( n = 20) or DMM‐operated ( n = 20) WT mice (12 weeks post‐surgery end timepoint) treated intraperitoneally with either IgG1 (vehicle control; 15 µg per mouse; daily for 12 weeks post‐surgery) or αIL‐33 (15 µg per mouse; daily for 12 weeks post‐surgery). (f) mRNA expression of cartilage degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in whole knee joints of DMM‐operated ( n = 20) treated intraperitoneally with either IgG1 (vehicle control; 15 µg per mouse; daily for 12 weeks post‐surgery) or αIL‐33 (15 µg per mouse; daily for 12 weeks post‐surgery). (g) protein and (h) mRNA expression of cartilage degrading proteases (MMP‐13, ADAMTS‐5 and MMP‐3) and chondrogenic markers (COL2A1, SOX‐9 and Aggrecan) in isolated human chondrocytes from Non‐OA ( n = 20) and OA patients ( n = 20) treated with rIL‐33 (30 ng mL −1 , 24 h) and IgG1 (vehicle control; 10 μg mL −1 , 24 h) or αIL‐33 (10 μg mL −1 , 24 h). (i) MMP‐13 ( j) MMP‐3 protein level in cell media supernatants obtained from isolated human chondrocytes from Non‐OA ( n = 12) and OA patients ( n = 12) treated with rIL‐33 (30 ng mL −1 ; 24 h) and IgG1 (vehicle control; 10 μg mL −1 , 24 h) or αIL‐33 (10 μg mL −1 , 24 h). All RT‐qPCR gene expressions were normalised to the endogenous level of 18 s in respective groups. Data are expressed as mean ± S.E.M. with two‐way analysis of variance followed by the Tukey‐Kramer test ( b, c, d ) or repeated measures 2‐way ANOVA with Bonferroni’s post hoc tests was used to compare groups at each time point ( e ; DMM IgG1 control mice vs DMM αIL‐33 mice) or with unpaired 2‐tailed Student’s t ‐tests ( i, j ). n indicates the number of human specimens or mice per group. NS = non‐significant. P < 0.0001 is represented as ****.

Article Snippet: For experiments which increased IL‐33 levels in vivo , mouse rIL‐33 (Enzo Life Sciences, Farmingdale) was administered intraperitoneally (i.p) on a daily basis at 33 μg kg −1 for 12 weeks post‐surgery.

Techniques: Expressing, Isolation, Quantitative RT-PCR