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Novus Biologicals mouse rankl monoclonal antibody
Mouse Rankl Monoclonal Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 20 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+rankl+monoclonal+antibody/pm41555413-80-0-8?v=Novus+Biologicals
Average 93 stars, based on 20 article reviews

mouse rankl monoclonal antibody - by Bioz Stars, 2026-07

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( A and B ) Ctsk –/– mice and control littermates were treated with intrapleural HAM and sacrificed on day 14, and pleural surface hydroxyproline ( A ) and adhesion scores ( B ) were determined as in Figure 1. ( C ) In separate experiments, mice were treated with intrapleural HAM and treated with control IgG or anti-RANKL mAb 3 times weekly over 28 days. μCT was performed, and HAM voxel density was estimated by quantitative methods as outlined in Figure 7. Data are shown as mean ± SD. Comparisons were by unpaired t test for 2 groups and by 1-way ANOVA followed by Tukey’s multiple-comparison test. * P < 0.05, ** P < 0.01, and *** P < 0.001

Journal: JCI Insight

Article Title: Hydroxyapatite microspheres induce durable pleurodesis and are rapidly cleared by pleural osteoclasts

doi: 10.1172/jci.insight.192981

Figure Lengend Snippet: ( A and B ) Ctsk –/– mice and control littermates were treated with intrapleural HAM and sacrificed on day 14, and pleural surface hydroxyproline ( A ) and adhesion scores ( B ) were determined as in Figure 1. ( C ) In separate experiments, mice were treated with intrapleural HAM and treated with control IgG or anti-RANKL mAb 3 times weekly over 28 days. μCT was performed, and HAM voxel density was estimated by quantitative methods as outlined in Figure 7. Data are shown as mean ± SD. Comparisons were by unpaired t test for 2 groups and by 1-way ANOVA followed by Tukey’s multiple-comparison test. * P < 0.05, ** P < 0.01, and *** P < 0.001

Article Snippet: C57BL/6J mice were treated with i.p. anti-mouse RANKL mAb (Bio-X-Cell, catalog BE0191, clone IK 22-5) or a Rat IgG2a isotype Control IgG (Bio-X-Cell, catalog BE0089, clone 2A-3) as reported , before being sacrificed 28 days after challenge, followed by assessments of particle density by μCT.

Techniques: Control, Comparison

The mRNA levels of receptor activator of nuclear factor-kappa B ligand and osteoprotegerin genes in each group. A and B: On the 3 rd , 7 th , 14 th , and 21 st day post-transfection, real-time quantitative polymerase chain reaction was used to evaluate the mRNA levels of osteoprotegerin (OPG) (A) and receptor activator of nuclear factor-kappa B ligand (RANKL) (B) in each group. The experimental group, “shOPG”, represents OPG gene-silenced bone marrow-derived mesenchymal stem cells (BMSCs) transfected with shOPG, while the control groups, “shScr” and “control”, represent BMSCs transfected with a scramble vector and untreated BMSCs, respectively. Compared to the shScr and control groups, RANKL was upregulated in shOPG-transfected BMSCs, particularly on day 3. Conversely, OPG expression was downregulated in shOPG-transfected BMSCs compared to the shScr and control groups (mean ± SEM, n = 3 experiments). a P < 0.05; b P < 0.01. BMSC: Bone marrow-derived mesenchymal stem cell; OPG: Osteoprotegerin; RANKL: Receptor activator of nuclear factor-kappa B ligand.

Journal: World Journal of Stem Cells

Article Title: RNA interference-mediated osteoprotegerin silencing increases the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio and promotes osteoclastogenesis

doi: 10.4252/wjsc.v17.i4.101290

Figure Lengend Snippet: The mRNA levels of receptor activator of nuclear factor-kappa B ligand and osteoprotegerin genes in each group. A and B: On the 3 rd , 7 th , 14 th , and 21 st day post-transfection, real-time quantitative polymerase chain reaction was used to evaluate the mRNA levels of osteoprotegerin (OPG) (A) and receptor activator of nuclear factor-kappa B ligand (RANKL) (B) in each group. The experimental group, “shOPG”, represents OPG gene-silenced bone marrow-derived mesenchymal stem cells (BMSCs) transfected with shOPG, while the control groups, “shScr” and “control”, represent BMSCs transfected with a scramble vector and untreated BMSCs, respectively. Compared to the shScr and control groups, RANKL was upregulated in shOPG-transfected BMSCs, particularly on day 3. Conversely, OPG expression was downregulated in shOPG-transfected BMSCs compared to the shScr and control groups (mean ± SEM, n = 3 experiments). a P < 0.05; b P < 0.01. BMSC: Bone marrow-derived mesenchymal stem cell; OPG: Osteoprotegerin; RANKL: Receptor activator of nuclear factor-kappa B ligand.

Article Snippet: Transfer the separated proteins to a polyvinylidene fluoride membrane (Abcam, ab133411) and incubate with mouse monoclonal antibodies against RANKL (SC 52950) and OPG (SC 390518) from Santa Cruz Biotechnology, CA, United States, and β-actin (CB100997M) mouse monoclonal antibody from California Bioscience, California, United States (diluted at 1:1000) following the manufacturer’s instructions, together (diluted at 1:200).

Techniques: Transfection, Real-time Polymerase Chain Reaction, Derivative Assay, Control, Plasmid Preparation, Expressing

Protein levels of receptor activator of nuclear factor-kappa B ligand and osteoprotegerin in each group. A and B: The western blot results of osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa B ligand (RANKL) protein expression at different time points (3 rd , 7 th , 14 th , and 21 st days) after transfection with shScr or shOPG (A) and their quantitative analysis (B). The experimental group, “shOPG”, represents OPG gene-silenced bone marrow-derived mesenchymal stem cells (BMSCs) transfected with shOPG, while the control groups, “shScr” and “control”, represent BMSCs transfected with a scramble vector and untreated BMSCs, respectively. The data represent results from three independent experiments. Changes in RANKL and OPG protein levels in shOPG-transfected BMSCs were observed compared to the shScr and control groups (mean ± SEM, n = 3 experiments). a P < 0.05; b P < 0.01. BMSC: Bone marrow-derived mesenchymal stem cell; OPG: Osteoprotegerin; RANKL: Receptor activator of nuclear factor-kappa B ligand.

Journal: World Journal of Stem Cells

Article Title: RNA interference-mediated osteoprotegerin silencing increases the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio and promotes osteoclastogenesis

doi: 10.4252/wjsc.v17.i4.101290

Figure Lengend Snippet: Protein levels of receptor activator of nuclear factor-kappa B ligand and osteoprotegerin in each group. A and B: The western blot results of osteoprotegerin (OPG) and receptor activator of nuclear factor-kappa B ligand (RANKL) protein expression at different time points (3 rd , 7 th , 14 th , and 21 st days) after transfection with shScr or shOPG (A) and their quantitative analysis (B). The experimental group, “shOPG”, represents OPG gene-silenced bone marrow-derived mesenchymal stem cells (BMSCs) transfected with shOPG, while the control groups, “shScr” and “control”, represent BMSCs transfected with a scramble vector and untreated BMSCs, respectively. The data represent results from three independent experiments. Changes in RANKL and OPG protein levels in shOPG-transfected BMSCs were observed compared to the shScr and control groups (mean ± SEM, n = 3 experiments). a P < 0.05; b P < 0.01. BMSC: Bone marrow-derived mesenchymal stem cell; OPG: Osteoprotegerin; RANKL: Receptor activator of nuclear factor-kappa B ligand.

Techniques: Western Blot, Expressing, Transfection, Derivative Assay, Control, Plasmid Preparation

Receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio of shOPG and shScr groups in mRNA and protein levels. A and B: Time-dependent changes in the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin (RANKL/OPG) mRNA (A) and protein (B) ratio following transfection with shScr or shOPG. The control group, “shScr”, represents bone marrow-derived mesenchymal stem cells transfected with a scramble vector, while the experimental group, “shOPG”, represents bone marrow-derived mesenchymal stem cells transfected with shOPG. Comparisons of RANKL/OPG mRNA and protein levels were conducted on the 3 rd , 7 th , 14 th , and 21 st days post-transfection between the “shOPG” and “shScr” groups. A comparison was made on the 3 rd , 7 th , 14 th , and 21 st days post-transduction with the control group. a P < 0.05; b P < 0.01 compared to the control group. OPG: Osteoprotegerin; RANKL: Receptor activator of nuclear factor-kappa B ligand.

Journal: World Journal of Stem Cells

Article Title: RNA interference-mediated osteoprotegerin silencing increases the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio and promotes osteoclastogenesis

doi: 10.4252/wjsc.v17.i4.101290

Figure Lengend Snippet: Receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio of shOPG and shScr groups in mRNA and protein levels. A and B: Time-dependent changes in the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin (RANKL/OPG) mRNA (A) and protein (B) ratio following transfection with shScr or shOPG. The control group, “shScr”, represents bone marrow-derived mesenchymal stem cells transfected with a scramble vector, while the experimental group, “shOPG”, represents bone marrow-derived mesenchymal stem cells transfected with shOPG. Comparisons of RANKL/OPG mRNA and protein levels were conducted on the 3 rd , 7 th , 14 th , and 21 st days post-transfection between the “shOPG” and “shScr” groups. A comparison was made on the 3 rd , 7 th , 14 th , and 21 st days post-transduction with the control group. a P < 0.05; b P < 0.01 compared to the control group. OPG: Osteoprotegerin; RANKL: Receptor activator of nuclear factor-kappa B ligand.

Techniques: Transfection, Control, Derivative Assay, Plasmid Preparation, Comparison, Transduction

Co-immunoprecipitation results of the interaction between receptor activator of nuclear factor-kappa B ligand and osteoprotegerin. This figure demonstrates the protein-protein interaction between receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG) in co-immunoprecipitation experiments. In the input samples (input, the supernatant obtained from centrifuged bone marrow-derived mesenchymal stem cell protein lysates without antibody addition or immunoprecipitation), distinct protein bands were observed at 55 kDa and 35 kDa, corresponding to OPG and RANKL, respectively. Significant bands were also detected at 55 kDa and 35 kDa in the immunoprecipitation samples using RANKL antibody (RANKL) and OPG antibody (OPG), indicating a direct protein-protein interaction between RANKL and OPG. No significant signals were observed in the negative control group (immunoglobulin G), confirming the specificity of the experimental results. n = 3. RANKL: Receptor activator of nuclear factor-kappa B ligand; OPG: Osteoprotegerin; IgG: Immunoglobulin G.

Journal: World Journal of Stem Cells

Article Title: RNA interference-mediated osteoprotegerin silencing increases the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio and promotes osteoclastogenesis

doi: 10.4252/wjsc.v17.i4.101290

Figure Lengend Snippet: Co-immunoprecipitation results of the interaction between receptor activator of nuclear factor-kappa B ligand and osteoprotegerin. This figure demonstrates the protein-protein interaction between receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG) in co-immunoprecipitation experiments. In the input samples (input, the supernatant obtained from centrifuged bone marrow-derived mesenchymal stem cell protein lysates without antibody addition or immunoprecipitation), distinct protein bands were observed at 55 kDa and 35 kDa, corresponding to OPG and RANKL, respectively. Significant bands were also detected at 55 kDa and 35 kDa in the immunoprecipitation samples using RANKL antibody (RANKL) and OPG antibody (OPG), indicating a direct protein-protein interaction between RANKL and OPG. No significant signals were observed in the negative control group (immunoglobulin G), confirming the specificity of the experimental results. n = 3. RANKL: Receptor activator of nuclear factor-kappa B ligand; OPG: Osteoprotegerin; IgG: Immunoglobulin G.

Techniques: Immunoprecipitation, Derivative Assay, Negative Control

Molecular mechanism of osteoprotegerin suppression in enhancing osteoclastogenesis via modulation of the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio. BMSC: Bone marrow-derived mesenchymal stem cell; OPG: Osteoprotegerin; RANKL: Receptor activator of nuclear factor-kappa B ligand; shRNA: Short hairpin RNA; TRAP: Tartrate-resistant acid phosphatase.

Journal: World Journal of Stem Cells

Article Title: RNA interference-mediated osteoprotegerin silencing increases the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio and promotes osteoclastogenesis

doi: 10.4252/wjsc.v17.i4.101290

Figure Lengend Snippet: Molecular mechanism of osteoprotegerin suppression in enhancing osteoclastogenesis via modulation of the receptor activator of nuclear factor-kappa B ligand/osteoprotegerin ratio. BMSC: Bone marrow-derived mesenchymal stem cell; OPG: Osteoprotegerin; RANKL: Receptor activator of nuclear factor-kappa B ligand; shRNA: Short hairpin RNA; TRAP: Tartrate-resistant acid phosphatase.

Techniques: Derivative Assay, shRNA

Supernatants from knee homogenates of NMRI mice on day 3 after intra-articular (i.a.) injection of 20 μL of PBS (healthy; n = 4) or Lpl1(+sp) or Lpl1(-sp) (4 μg/knee; n = 5/group) were assessed for the levels of CCL2 (MCP-1, A ), MCSF ( B ), and RANKL ( C ) by ELISA. Levels of CCL2 (MCP-1, D ), MCSF ( E ), and RANKL ( F ) in the supernatants from knee homogenates of NMRI mice on day 3 after i.a. injection of 20 μL of PBS (healthy; n = 4) or the synthetic lipopeptides, P2C or P3C (4 μg/knee; n = 4 to 6/group). Levels of CCL2 (MCP-1, G ), MCSF ( H ), and RANKL ( I ) in the supernatants from knee homogenates of NMRI mice depleted of monocytes/macrophages using clodronate liposomes (Monocyte depletion) or PBS control liposomes (Control) on day 3 after i.a. injection of 20 μL of P2C (4 μg/knee; n = 6/group). Data were pooled from 2 independent experiments. Mouse knee synovial fibroblasts were stimulated with P2C or P3C (20 ng/mL; n = 5/group), or Lpl1(+sp) or Lpl1(-sp) (0.2 μg/mL; n = 5/group) for 48 hours. The expression levels of RANKL were analyzed with the TaqMan assay, and the relative gene expression was calculated using the ΔCt method ( J ). The fold-changes in gene expression levels were normalized against medium-only samples ( K ). Statistical evaluations were performed using 1-way ANOVA with Tukey’s multiple-comparison test ( A – I ), repeated measures 1-way ANOVA with Dunnett’s multiple-comparison test ( J ), and the Mann-Whitney test ( K ), with the data presented as mean with SEM. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: JCI Insight

Article Title: Combination treatment with anti-RANKL and antibiotics for preventing joint destruction in septic arthritis

doi: 10.1172/jci.insight.184954

Figure Lengend Snippet: Supernatants from knee homogenates of NMRI mice on day 3 after intra-articular (i.a.) injection of 20 μL of PBS (healthy; n = 4) or Lpl1(+sp) or Lpl1(-sp) (4 μg/knee; n = 5/group) were assessed for the levels of CCL2 (MCP-1, A ), MCSF ( B ), and RANKL ( C ) by ELISA. Levels of CCL2 (MCP-1, D ), MCSF ( E ), and RANKL ( F ) in the supernatants from knee homogenates of NMRI mice on day 3 after i.a. injection of 20 μL of PBS (healthy; n = 4) or the synthetic lipopeptides, P2C or P3C (4 μg/knee; n = 4 to 6/group). Levels of CCL2 (MCP-1, G ), MCSF ( H ), and RANKL ( I ) in the supernatants from knee homogenates of NMRI mice depleted of monocytes/macrophages using clodronate liposomes (Monocyte depletion) or PBS control liposomes (Control) on day 3 after i.a. injection of 20 μL of P2C (4 μg/knee; n = 6/group). Data were pooled from 2 independent experiments. Mouse knee synovial fibroblasts were stimulated with P2C or P3C (20 ng/mL; n = 5/group), or Lpl1(+sp) or Lpl1(-sp) (0.2 μg/mL; n = 5/group) for 48 hours. The expression levels of RANKL were analyzed with the TaqMan assay, and the relative gene expression was calculated using the ΔCt method ( J ). The fold-changes in gene expression levels were normalized against medium-only samples ( K ). Statistical evaluations were performed using 1-way ANOVA with Tukey’s multiple-comparison test ( A – I ), repeated measures 1-way ANOVA with Dunnett’s multiple-comparison test ( J ), and the Mann-Whitney test ( K ), with the data presented as mean with SEM. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Article Snippet: Monoclonal anti-RANKL antibody (clone IK22/5; BioXCell) ( ) and anti-mouse CSF1R antibody (clone AFS98; BioXCell) ( ) were utilized to inhibit murine RANKL and MCSFR (also known as CSF1R), respectively.

Techniques: Injection, Enzyme-linked Immunosorbent Assay, Liposomes, Control, Expressing, TaqMan Assay, Gene Expression, Comparison, MANN-WHITNEY

( A ) Measurement of knee swelling (in mm, n = 10/group) of NMRI mice treated with anti-mouse CSF1R antibodies (anti-MCSFR) or an isotype control (Controls), administered 3 hours prior to intra-articular (i.a.) infection of 20 μL of PBS containing S . aureus LS-1 strain (4 × 10 3 CFU/knee). ( B ) Bacterial counts of S . aureus in mouse knee joints ( n = 5/group) and ( C ) bone erosion scores of mouse knee joints ( n = 5/group) were determined after μCT scan on day 10 after the mice were sacrificed. ( D ) Knee swelling measurements (in mm, n = 10/group) of NMRI mice treated with anti-mouse RANKL antibodies (anti-RANKL) or an isotype control (Controls), administered 1 day prior to i.a. infection of 20 μL of PBS containing S . aureus LS-1 strain (4 × 10 3 CFU/knee). ( E ) Bacterial counts ( n = 5/group) and ( F ) bone erosion scores ( n = 5/group) were determined after μCT scan on day 10 after the mice were sacrificed. To mimic more accurately the clinical progress, additional assessments were conducted with varied administration timing, 2 days after infection ( G – I ), and ( J ) representative μCT images are shown. Arrows indicate bone erosion. ( K ) Representative TRAP staining images of mouse knee joints that received injections of PBS, isotype control antibody, or anti-RANKL antibody. The insets (lower panels) represent higher magnification images of the boxed areas, with the arrows indicating TRAP-positive cells. Scale bar: 100 μm. Statistical evaluations were performed using the Mann-Whitney test, and the data are presented as mean with SEM. * P < 0.05; ** P < 0.01.

Journal: JCI Insight

Article Title: Combination treatment with anti-RANKL and antibiotics for preventing joint destruction in septic arthritis

doi: 10.1172/jci.insight.184954

Figure Lengend Snippet: ( A ) Measurement of knee swelling (in mm, n = 10/group) of NMRI mice treated with anti-mouse CSF1R antibodies (anti-MCSFR) or an isotype control (Controls), administered 3 hours prior to intra-articular (i.a.) infection of 20 μL of PBS containing S . aureus LS-1 strain (4 × 10 3 CFU/knee). ( B ) Bacterial counts of S . aureus in mouse knee joints ( n = 5/group) and ( C ) bone erosion scores of mouse knee joints ( n = 5/group) were determined after μCT scan on day 10 after the mice were sacrificed. ( D ) Knee swelling measurements (in mm, n = 10/group) of NMRI mice treated with anti-mouse RANKL antibodies (anti-RANKL) or an isotype control (Controls), administered 1 day prior to i.a. infection of 20 μL of PBS containing S . aureus LS-1 strain (4 × 10 3 CFU/knee). ( E ) Bacterial counts ( n = 5/group) and ( F ) bone erosion scores ( n = 5/group) were determined after μCT scan on day 10 after the mice were sacrificed. To mimic more accurately the clinical progress, additional assessments were conducted with varied administration timing, 2 days after infection ( G – I ), and ( J ) representative μCT images are shown. Arrows indicate bone erosion. ( K ) Representative TRAP staining images of mouse knee joints that received injections of PBS, isotype control antibody, or anti-RANKL antibody. The insets (lower panels) represent higher magnification images of the boxed areas, with the arrows indicating TRAP-positive cells. Scale bar: 100 μm. Statistical evaluations were performed using the Mann-Whitney test, and the data are presented as mean with SEM. * P < 0.05; ** P < 0.01.

Techniques: Control, Infection, Staining, MANN-WHITNEY

NMRI mice ( n = 5/group) received anti-RANKL treatment or the isotype control 1 day prior to intravenous infection with S . aureus Newman strain (5 × 10 6 CFU/mouse) and were sacrificed on day 10 after infection. The arthritis severities ( A ) and bacterial loads in the kidneys ( B ). Cumulative bone destruction scores ( C ) and frequencies of bone destruction ( D ) of the joints from all 4 limbs were assessed by μCT scan. Additional assessments with administration timing, 2 days after infection ( E – H ), were conducted to mimic more closely the clinical progress. Representative μCT images are presented that show both control (left) and anti-RANKL–treated (right) mouse joints, ( I ) hind paws, ( J ) wrists, and ( K ) knees. Arrows indicate the bone erosion. Data are reported as mean ± SEM and analyzed with the Mann-Whitney test ( A – C and E – G ) or Fisher’s exact test ( D and H ). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Journal: JCI Insight

Article Title: Combination treatment with anti-RANKL and antibiotics for preventing joint destruction in septic arthritis

doi: 10.1172/jci.insight.184954

Figure Lengend Snippet: NMRI mice ( n = 5/group) received anti-RANKL treatment or the isotype control 1 day prior to intravenous infection with S . aureus Newman strain (5 × 10 6 CFU/mouse) and were sacrificed on day 10 after infection. The arthritis severities ( A ) and bacterial loads in the kidneys ( B ). Cumulative bone destruction scores ( C ) and frequencies of bone destruction ( D ) of the joints from all 4 limbs were assessed by μCT scan. Additional assessments with administration timing, 2 days after infection ( E – H ), were conducted to mimic more closely the clinical progress. Representative μCT images are presented that show both control (left) and anti-RANKL–treated (right) mouse joints, ( I ) hind paws, ( J ) wrists, and ( K ) knees. Arrows indicate the bone erosion. Data are reported as mean ± SEM and analyzed with the Mann-Whitney test ( A – C and E – G ) or Fisher’s exact test ( D and H ). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001.

Techniques: Control, Infection, MANN-WHITNEY

NMRI mice ( n = 5/group) were intravenously injected with S . aureus Newman strain (5 × 10 6 CFU/mouse) and sacrificed on day 14 after infection. The following treatments were administered intraperitoneally twice daily commencing on day 5 after infection to the respective groups: isotype antibodies with PBS, anti-RANKL antibodies with PBS, isotype antibodies with cloxacillin, and anti-RANKL antibodies with cloxacillin. ( A ) The changes in body weight, ( B ) arthritis severities, ( C ) cumulative survival, ( D ) bacterial loads in the kidneys, ( E ) cumulative bone destruction scores, and ( F ) frequencies of bone destruction of the joints from all 4 limbs were assessed by μCT scan. Data are presented as mean with SEM. Statistical evaluations were performed using 2-way ANOVA with Tukey’s multiple-comparison test ( A and B ), log-rank (Mantel-Cox) test ( C ), 1-way ANOVA with Holm-Šídák multiple-comparison test ( D ), Kruskal-Wallis test with Dunn’s multiple-comparison test ( E ), or Fisher’s exact test ( F ). a, anti-RANKL + PBS vs. anti-RANKL + cloxacillin; b, anti-RANKL + PBS vs. isotype control + cloxacillin; c, anti-RANKL + cloxacillin vs. isotype control + PBS; d, isotype control + cloxacillin vs. isotype control + PBS. * P < 0.05; ** P < 0.01; *** P < 0.001.

Journal: JCI Insight

Article Title: Combination treatment with anti-RANKL and antibiotics for preventing joint destruction in septic arthritis

doi: 10.1172/jci.insight.184954

Figure Lengend Snippet: NMRI mice ( n = 5/group) were intravenously injected with S . aureus Newman strain (5 × 10 6 CFU/mouse) and sacrificed on day 14 after infection. The following treatments were administered intraperitoneally twice daily commencing on day 5 after infection to the respective groups: isotype antibodies with PBS, anti-RANKL antibodies with PBS, isotype antibodies with cloxacillin, and anti-RANKL antibodies with cloxacillin. ( A ) The changes in body weight, ( B ) arthritis severities, ( C ) cumulative survival, ( D ) bacterial loads in the kidneys, ( E ) cumulative bone destruction scores, and ( F ) frequencies of bone destruction of the joints from all 4 limbs were assessed by μCT scan. Data are presented as mean with SEM. Statistical evaluations were performed using 2-way ANOVA with Tukey’s multiple-comparison test ( A and B ), log-rank (Mantel-Cox) test ( C ), 1-way ANOVA with Holm-Šídák multiple-comparison test ( D ), Kruskal-Wallis test with Dunn’s multiple-comparison test ( E ), or Fisher’s exact test ( F ). a, anti-RANKL + PBS vs. anti-RANKL + cloxacillin; b, anti-RANKL + PBS vs. isotype control + cloxacillin; c, anti-RANKL + cloxacillin vs. isotype control + PBS; d, isotype control + cloxacillin vs. isotype control + PBS. * P < 0.05; ** P < 0.01; *** P < 0.001.

Techniques: Injection, Infection, Comparison, Control

Schematic delineating the key steps in preventing bone destruction during septic arthritis. In the complex cascade that leads to bone damage, the recruitment of Ly6C hi monocytes emerges as a pivotal event in the initiation of bone damage. S . aureus Lpps exert profound impacts on the upregulation of molecules associated with bone destruction. Targeting the RANKL proves to be effective in preventing bone damage in both locally induced and hematogenous septic arthritis models. The approach using anti-RANKL in combination with cloxacillin treatment synergistically shields against bone destruction, posing a potentially novel strategy to combat septic arthritis–induced bone damage.

Journal: JCI Insight

Article Title: Combination treatment with anti-RANKL and antibiotics for preventing joint destruction in septic arthritis

doi: 10.1172/jci.insight.184954

Figure Lengend Snippet: Schematic delineating the key steps in preventing bone destruction during septic arthritis. In the complex cascade that leads to bone damage, the recruitment of Ly6C hi monocytes emerges as a pivotal event in the initiation of bone damage. S . aureus Lpps exert profound impacts on the upregulation of molecules associated with bone destruction. Targeting the RANKL proves to be effective in preventing bone damage in both locally induced and hematogenous septic arthritis models. The approach using anti-RANKL in combination with cloxacillin treatment synergistically shields against bone destruction, posing a potentially novel strategy to combat septic arthritis–induced bone damage.

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