cytokine concentrations  (Elabscience Biotechnology)

Journal: Frontiers in Immunology

Article Title: Targeting neuroinflammation: itaconate and mesaconate as therapeutic strategies against H7N7 influenza-associated CNS damage

doi: 10.3389/fimmu.2026.1776302

Figure Lengend Snippet: Limited effects of itaconate and mesaconate on H7N7-induced inflammatory mediator production in lung and brain at 8 dpi. Pro-inflammatory cytokine levels were quantified by ELISA in lung (A–D) and brain (E–H) tissues from PBS-inoculated control and H7N7-infected mice treated with PBS, itaconate, or mesaconate at 8 dpi. (A–D) H7N7 infection induced robust pulmonary increases in IL-6 (B) , IL-1β (C) , and IFN-γ (D) , which were not attenuated by either metabolite treatment. (E–H) In the brain, H7N7 infection increased IL-6 (F) and IL-1β (G) levels, with itaconate treatment further enhancing TNF-α production (E) , whereas mesaconate treatment was associated with reduced IL-1β (G) and attenuated neuroinflammatory responses. Data are presented as mean ± SEM. Statistical analysis was performed using two-way ANOVA followed by Fisher’s LSD post hoc test (* p < 0.05, ** p < 0.01 and *** p < 0.001). Group sizes ranged from N = 3–5 mice per group.

Article Snippet: Pro-inflammatory cytokine concentrations (TNF-α: Cat. # DY410, assay range: 31.2–2000 pg/mL; IL-6: Cat. # DY406, assay range: 15.6–1000 pg/mL; IL-1β: Cat. # DY401, assay range: 15.6–1000 pg/mL and IFN-γ: Cat. # DY485, assay range: 31.2–2000 pg/mL) were quantified using DuoSet ELISA kits (R&D Systems) according to the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay, Control, Infection

Journal: Frontiers in Immunology

Article Title: Targeting neuroinflammation: itaconate and mesaconate as therapeutic strategies against H7N7 influenza-associated CNS damage

doi: 10.3389/fimmu.2026.1776302

Figure Lengend Snippet: Proposed model of immunometabolic modulation during neurotropic IAV infection. The schematic illustrates that following IAV infection, (1) pro-inflammatory cytokines released by activated peripheral monocytes and macrophages and/or viral particles themselves can access the brain and trigger neuroinflammatory responses. Whether in vivo treatment with itaconate or mesaconate directly inhibits viral replication remains unknown. (2) Mesaconate selectively reduced brain IL-1β and IL-6 levels, whereas itaconate (3) more robustly suppressed infection-induced microglial density and activation and attenuated (4) microglial morphological reactivity and synaptic remodeling associated with infection, (5) processes that are implicated in subsequent neurodegenerative changes. Collectively, the model supports emerging evidence that structurally related itaconate isomers engage partially overlapping yet mechanistically distinct signaling programs rather than differing solely in inhibitory potency ( Created in BioRender. https://BioRender.com/pqfhoem , is licensed under CC BY 4.0 ).

Article Snippet: Pro-inflammatory cytokine concentrations (TNF-α: Cat. # DY410, assay range: 31.2–2000 pg/mL; IL-6: Cat. # DY406, assay range: 15.6–1000 pg/mL; IL-1β: Cat. # DY401, assay range: 15.6–1000 pg/mL and IFN-γ: Cat. # DY485, assay range: 31.2–2000 pg/mL) were quantified using DuoSet ELISA kits (R&D Systems) according to the manufacturer’s instructions.

Techniques: Infection, In Vivo, Activation Assay