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lfn rod  (InvivoGen)


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    Structured Review

    InvivoGen lfn rod
    RANKL-exposed macrophages produce fewer proinflammatory cytokines. Primary mouse BMDMs were treated with 0 or 100 ng/mL RANKL and M-CSF for 2 d before being infected with S Tm SL1344 at an MOI of 1, mock infected, or stimulated with ultrapure LPS. At the indicated time points, supernatants were assayed for (A) TNF-α, (B) IL-1β, or (D) IL-6 via enzyme-linked immunosorbent assay. (C) To stimulate the NLRP3 inflammasome, BMDMs primed with LPS for 23.5 h were treated with nigericin or ATP for 30 min. To stimulate the NLRC4 inflammasome, BMDMs were treated <t>with</t> <t>LFn-Rod</t> and protective antigen for 24 h. Supernatant IL-1β was assayed by enzyme-linked immunosorbent assay. Data represent mean ± SEM from 3 independent experiments (2-way analysis of variance with Holm-Šidák multiple comparisons test). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. ns, not significant.
    Lfn Rod, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/lfn-rod/LFn-Rod/pmc13198865-102-11-12
    Average 94 stars, based on 10 article reviews
    lfn rod - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "RANKL inhibits macrophage proinflammatory Toll-like receptor 2 and 4 signaling and impairs killing of intracellular bacteria"

    Article Title: RANKL inhibits macrophage proinflammatory Toll-like receptor 2 and 4 signaling and impairs killing of intracellular bacteria

    Journal: ImmunoHorizons

    doi: 10.1093/immhor/vlag023

    RANKL-exposed macrophages produce fewer proinflammatory cytokines. Primary mouse BMDMs were treated with 0 or 100 ng/mL RANKL and M-CSF for 2 d before being infected with S Tm SL1344 at an MOI of 1, mock infected, or stimulated with ultrapure LPS. At the indicated time points, supernatants were assayed for (A) TNF-α, (B) IL-1β, or (D) IL-6 via enzyme-linked immunosorbent assay. (C) To stimulate the NLRP3 inflammasome, BMDMs primed with LPS for 23.5 h were treated with nigericin or ATP for 30 min. To stimulate the NLRC4 inflammasome, BMDMs were treated with LFn-Rod and protective antigen for 24 h. Supernatant IL-1β was assayed by enzyme-linked immunosorbent assay. Data represent mean ± SEM from 3 independent experiments (2-way analysis of variance with Holm-Šidák multiple comparisons test). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. ns, not significant.
    Figure Legend Snippet: RANKL-exposed macrophages produce fewer proinflammatory cytokines. Primary mouse BMDMs were treated with 0 or 100 ng/mL RANKL and M-CSF for 2 d before being infected with S Tm SL1344 at an MOI of 1, mock infected, or stimulated with ultrapure LPS. At the indicated time points, supernatants were assayed for (A) TNF-α, (B) IL-1β, or (D) IL-6 via enzyme-linked immunosorbent assay. (C) To stimulate the NLRP3 inflammasome, BMDMs primed with LPS for 23.5 h were treated with nigericin or ATP for 30 min. To stimulate the NLRC4 inflammasome, BMDMs were treated with LFn-Rod and protective antigen for 24 h. Supernatant IL-1β was assayed by enzyme-linked immunosorbent assay. Data represent mean ± SEM from 3 independent experiments (2-way analysis of variance with Holm-Šidák multiple comparisons test). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. ns, not significant.

    Techniques Used: Infection, Enzyme-linked Immunosorbent Assay



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    Image Search Results


    RANKL-exposed macrophages produce fewer proinflammatory cytokines. Primary mouse BMDMs were treated with 0 or 100 ng/mL RANKL and M-CSF for 2 d before being infected with S Tm SL1344 at an MOI of 1, mock infected, or stimulated with ultrapure LPS. At the indicated time points, supernatants were assayed for (A) TNF-α, (B) IL-1β, or (D) IL-6 via enzyme-linked immunosorbent assay. (C) To stimulate the NLRP3 inflammasome, BMDMs primed with LPS for 23.5 h were treated with nigericin or ATP for 30 min. To stimulate the NLRC4 inflammasome, BMDMs were treated with LFn-Rod and protective antigen for 24 h. Supernatant IL-1β was assayed by enzyme-linked immunosorbent assay. Data represent mean ± SEM from 3 independent experiments (2-way analysis of variance with Holm-Šidák multiple comparisons test). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. ns, not significant.

    Journal: ImmunoHorizons

    Article Title: RANKL inhibits macrophage proinflammatory Toll-like receptor 2 and 4 signaling and impairs killing of intracellular bacteria

    doi: 10.1093/immhor/vlag023

    Figure Lengend Snippet: RANKL-exposed macrophages produce fewer proinflammatory cytokines. Primary mouse BMDMs were treated with 0 or 100 ng/mL RANKL and M-CSF for 2 d before being infected with S Tm SL1344 at an MOI of 1, mock infected, or stimulated with ultrapure LPS. At the indicated time points, supernatants were assayed for (A) TNF-α, (B) IL-1β, or (D) IL-6 via enzyme-linked immunosorbent assay. (C) To stimulate the NLRP3 inflammasome, BMDMs primed with LPS for 23.5 h were treated with nigericin or ATP for 30 min. To stimulate the NLRC4 inflammasome, BMDMs were treated with LFn-Rod and protective antigen for 24 h. Supernatant IL-1β was assayed by enzyme-linked immunosorbent assay. Data represent mean ± SEM from 3 independent experiments (2-way analysis of variance with Holm-Šidák multiple comparisons test). * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001. ns, not significant.

    Article Snippet: To stimulate the NLRC4 inflammasome, BMDMs were treated with 2 μg/mL LFn-Rod (InvivoGen) and 1 μg/mL protective antigen (InvivoGen) in unsupplemented MEM-α with 1% GlutaMAX.

    Techniques: Infection, Enzyme-linked Immunosorbent Assay