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mouse il 18 duoset elisa kit  (R&D Systems)


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    R&D Systems mouse il 18 duoset elisa kit
    Mouse Il 18 Duoset Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 90 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/il+18+mouse+il+18+duoset+kit/Mouse+IL-18+DuoSet+ELISA/pm42018556-92-7-13
    Average 95 stars, based on 90 article reviews
    mouse il 18 duoset elisa kit - by Bioz Stars, 2026-10
    95/100 stars

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    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM 2.5 )-primed macrophages.
    Article Snippet: Data processing was performed with the LAS X Life Science software List of abbreviations ASC Apoptosis-associated speck-like protein containing a CARD BMDMs Bone marrow-derived macrophages CAPs Concentrated Air Particles NLRP3 NOD- LRR- and pyrin domain-containing protein 3 O2•- Superoxide anion PBMCs Peripheral blood mononuclear cells PM2.5 Fine particulate matter ROFA Residual Oil Fly Ash SRM Standard Reference Material L. Caceres et al. Environmental Pollution 341 (2024) 122997 (Leica Microsystems). .. IL-1β and IL-18 were quantified by ELISA in cell culture supernatants using the Human or Mouse IL-1β/IL-1F2 Quantikine Kit (R&D Systems), or the IL-18 Mouse IL-18 DuoSet kit (R&D Systems). .. TNF-α, IL-6, and CCL2 levels were quantified by the CBA Mouse Inflammation Kit (BD Biosciences) in cell culture supernatants according to manufacturer’s instructions.

    Article Title: Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM 2.5 )-primed macrophages
    Article Snippet: Data processing was performed with the LAS X Life Science software (Leica Microsystems). .. IL-1β and IL-18 were quantified by ELISA in cell culture supernatants using the Human or Mouse IL-1β/IL-1F2 Quantikine Kit (R&D Systems), or the IL-18 Mouse IL-18 DuoSet kit (R&D Systems). .. TNF-α, IL-6, and CCL2 levels were quantified by the CBA Mouse Inflammation Kit (BD Biosciences) in cell culture supernatants according to manufacturer's instructions.

    Cell Culture:

    Article Title: Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM 2.5 )-primed macrophages.
    Article Snippet: Data processing was performed with the LAS X Life Science software List of abbreviations ASC Apoptosis-associated speck-like protein containing a CARD BMDMs Bone marrow-derived macrophages CAPs Concentrated Air Particles NLRP3 NOD- LRR- and pyrin domain-containing protein 3 O2•- Superoxide anion PBMCs Peripheral blood mononuclear cells PM2.5 Fine particulate matter ROFA Residual Oil Fly Ash SRM Standard Reference Material L. Caceres et al. Environmental Pollution 341 (2024) 122997 (Leica Microsystems). .. IL-1β and IL-18 were quantified by ELISA in cell culture supernatants using the Human or Mouse IL-1β/IL-1F2 Quantikine Kit (R&D Systems), or the IL-18 Mouse IL-18 DuoSet kit (R&D Systems). .. TNF-α, IL-6, and CCL2 levels were quantified by the CBA Mouse Inflammation Kit (BD Biosciences) in cell culture supernatants according to manufacturer’s instructions.

    Article Title: Molecular mechanisms underlying NLRP3 inflammasome activation and IL-1β production in air pollution fine particulate matter (PM 2.5 )-primed macrophages
    Article Snippet: Data processing was performed with the LAS X Life Science software (Leica Microsystems). .. IL-1β and IL-18 were quantified by ELISA in cell culture supernatants using the Human or Mouse IL-1β/IL-1F2 Quantikine Kit (R&D Systems), or the IL-18 Mouse IL-18 DuoSet kit (R&D Systems). .. TNF-α, IL-6, and CCL2 levels were quantified by the CBA Mouse Inflammation Kit (BD Biosciences) in cell culture supernatants according to manufacturer's instructions.



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    mouse il 18 duoset elisa kit  (R&D Systems)
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    Mouse Il 18 Duoset Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and <t>IL-6/IL-18.</t> (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.
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    mouse il 18 elisa kit  (R&D Systems)
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    Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and <t>IL-6/IL-18.</t> (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.
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    Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and <t>IL-6/IL-18.</t> (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.
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    ADSC-Exos mitigate NLRP3-mediated pyroptosis in KA-induced temporal lobe epilepsy. (A–F) Western blot analysis and quantification of (A) representative immunoblots and protein levels of (B) NLRP3, (C) GSDMD-FL, (D) GSDMD-N, (E) Caspase-1, and <t>(F)</t> <t>IL-1β</t> in the Control, KA, KA+ADSC-Exos, and KA+Nig+ADSC-Exos groups. (G–J) qRT-PCR analysis of relative mRNA expression of (G) NLRP3, (H) GSDMD, (I) Caspase-1, and (J) IL-1β. (K–L) <t>ELISA</t> quantification of (K) serum IL-1β and (L) IL-18 levels. Individual data points represent values from each mouse (n=5 per group). Data are expressed as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (one-way ANOVA with Tukey’s post hoc test).
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    ADSC-Exos mitigate NLRP3-mediated pyroptosis in KA-induced temporal lobe epilepsy. (A–F) Western blot analysis and quantification of (A) representative immunoblots and protein levels of (B) NLRP3, (C) GSDMD-FL, (D) GSDMD-N, (E) Caspase-1, and <t>(F)</t> <t>IL-1β</t> in the Control, KA, KA+ADSC-Exos, and KA+Nig+ADSC-Exos groups. (G–J) qRT-PCR analysis of relative mRNA expression of (G) NLRP3, (H) GSDMD, (I) Caspase-1, and (J) IL-1β. (K–L) <t>ELISA</t> quantification of (K) serum IL-1β and (L) IL-18 levels. Individual data points represent values from each mouse (n=5 per group). Data are expressed as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (one-way ANOVA with Tukey’s post hoc test).
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    Image Search Results


    Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and IL-6/IL-18. (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.

    Journal: bioRxiv

    Article Title: Hippocampal Neuroinflammation and Altered Peripheral Neurobiological Protein Profile in Experimental Arthritis and Systemic Juvenile Idiopathic Arthritis

    doi: 10.64898/2026.03.13.711607

    Figure Lengend Snippet: Inflammatory profiles of sJIA patients and neuro–inflammation co-analysis reveal correlations between HMOX2 and IL-6/IL-18. (A) PCA plot of inflammation-related plasma proteins showing separation between active sJIA patients and HCs. Each point represents one subject (n = 32; 16 active sJIA and 16 HCs). (B) Volcano plot of DEPs in active sJIA vs. HC. Dashed lines indicate significance thresholds. (C) Volcano plot of DEPs in Cluster 2 active sJIA vs. Cluster 1 active sJIA. Dashed lines indicate significance thresholds. (D) PCA plot of inflammation related plasma proteins showing the distribution of sJIA patients (active vs inactive) and HCs. Each point represents one subject, with lines connecting paired active and inactive samples from the same patient (n = 36; 12 active sJIA, 12 inactive sJIA, and 12 HCs). (E) Bubble plot showing correlations between DEPs from the inflammation panel and DEPs from the neuro panel in active sJIA patients. (F) Correlation analysis showing significant negative correlations between HMOX2 and IL-6/IL-18. (G-H) Line plot showing longitudinal changes of IL-6 and IL-18 from healthy to active to inactive sJIA. Statistics: (B) paired t-test with Benjamini–Hochberg correction for multiple comparisons; (C) unpaired t-test with Benjamini–Hochberg correction for multiple comparisons; (E, F) Pearson correlation analysis; (G, H) Multiple paired t-tests with Holm–Bonferroni adjustment.

    Article Snippet: Mouse serum samples were also used to measure IL-6 and IL-18 level using IL-6 and IL-18 mouse Elisa kits (R&D systems, USA).

    Techniques: Clinical Proteomics

    IL-6 and IL-18 are elevated in arthritic mice and synergistically trigger oxidative stress in microglia. (A) Box plots showing increased serum IL-6 and IL-18 levels in arthritic mice. (B) Correlation analysis showing a negative correlation between serum IL-18 and HMOX2, whereas IL-6 showed no significant correlation in arthritic mice. (C) Scatter plots showing the correlations between serum IL-18/IL-6 and microglial activation in arthritic mice. (D–E) Representative images of DCFH-DA staining showing ROS levels in SimA9 cells treated with IL-6, IL-18, or both for 24 h, with corresponding quantification of fluorescence intensity. Scale Bar: 50μm. (F) ELISA results showing downregulation of extracellular HMOX2 in SimA9 cells following IL-18 treatment or IL-6/IL-18 co-treatment. Statistics: (A) unpaired t-test; (B, C) Spearman correlation analysis; (E, F) three independent experiments, one-way ANOVA followed by Tukey’s multiple comparisons test to assess differences among groups.

    Journal: bioRxiv

    Article Title: Hippocampal Neuroinflammation and Altered Peripheral Neurobiological Protein Profile in Experimental Arthritis and Systemic Juvenile Idiopathic Arthritis

    doi: 10.64898/2026.03.13.711607

    Figure Lengend Snippet: IL-6 and IL-18 are elevated in arthritic mice and synergistically trigger oxidative stress in microglia. (A) Box plots showing increased serum IL-6 and IL-18 levels in arthritic mice. (B) Correlation analysis showing a negative correlation between serum IL-18 and HMOX2, whereas IL-6 showed no significant correlation in arthritic mice. (C) Scatter plots showing the correlations between serum IL-18/IL-6 and microglial activation in arthritic mice. (D–E) Representative images of DCFH-DA staining showing ROS levels in SimA9 cells treated with IL-6, IL-18, or both for 24 h, with corresponding quantification of fluorescence intensity. Scale Bar: 50μm. (F) ELISA results showing downregulation of extracellular HMOX2 in SimA9 cells following IL-18 treatment or IL-6/IL-18 co-treatment. Statistics: (A) unpaired t-test; (B, C) Spearman correlation analysis; (E, F) three independent experiments, one-way ANOVA followed by Tukey’s multiple comparisons test to assess differences among groups.

    Article Snippet: Mouse serum samples were also used to measure IL-6 and IL-18 level using IL-6 and IL-18 mouse Elisa kits (R&D systems, USA).

    Techniques: Activation Assay, Staining, Fluorescence, Enzyme-linked Immunosorbent Assay

    ADSC-Exos mitigate NLRP3-mediated pyroptosis in KA-induced temporal lobe epilepsy. (A–F) Western blot analysis and quantification of (A) representative immunoblots and protein levels of (B) NLRP3, (C) GSDMD-FL, (D) GSDMD-N, (E) Caspase-1, and (F) IL-1β in the Control, KA, KA+ADSC-Exos, and KA+Nig+ADSC-Exos groups. (G–J) qRT-PCR analysis of relative mRNA expression of (G) NLRP3, (H) GSDMD, (I) Caspase-1, and (J) IL-1β. (K–L) ELISA quantification of (K) serum IL-1β and (L) IL-18 levels. Individual data points represent values from each mouse (n=5 per group). Data are expressed as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (one-way ANOVA with Tukey’s post hoc test).

    Journal: Frontiers in Immunology

    Article Title: Adipose-derived stem cell exosomes suppress NLRP3-mediated neuronal pyroptosis to attenuate seizures in a kainic acid-induced temporal lobe epilepsy model

    doi: 10.3389/fimmu.2025.1691814

    Figure Lengend Snippet: ADSC-Exos mitigate NLRP3-mediated pyroptosis in KA-induced temporal lobe epilepsy. (A–F) Western blot analysis and quantification of (A) representative immunoblots and protein levels of (B) NLRP3, (C) GSDMD-FL, (D) GSDMD-N, (E) Caspase-1, and (F) IL-1β in the Control, KA, KA+ADSC-Exos, and KA+Nig+ADSC-Exos groups. (G–J) qRT-PCR analysis of relative mRNA expression of (G) NLRP3, (H) GSDMD, (I) Caspase-1, and (J) IL-1β. (K–L) ELISA quantification of (K) serum IL-1β and (L) IL-18 levels. Individual data points represent values from each mouse (n=5 per group). Data are expressed as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 (one-way ANOVA with Tukey’s post hoc test).

    Article Snippet: IL-1β and IL-18 levels in mouse serum were measured using ELISA kits (R&D Systems, CatNo: DY401,DY122-05) following the manufacturer’s protocol.

    Techniques: Western Blot, Control, Quantitative RT-PCR, Expressing, Enzyme-linked Immunosorbent Assay