e. coli serotype o11  (InvivoGen)

Journal: International Dental Journal

Article Title: FAM30A Induces Inflammation and Oxidative Damage in PDLSCs by Targeting miR-424-5p

doi: 10.1016/j.identj.2026.109605

Figure Lengend Snippet: Effects of si- FAM30A on LPS-induced PDLSCs function and inflammatory levels. ( A) Exploration of optimal LPS concentration for inducing PDLSCs. ( B) Establishment of FAM30A knockdown cell lines. ( C) Effects of si- FAM30A transfection on PDLSCs proliferation. ( D) Apoptotic changes in PDLSCs following FAM30A inhibition. ( E) Expression of inflammatory-associated factors (TNF-α, IL-1β, IL-10) in PDLSCs following si- FAM30A transfection. ( F-H) Levels of oxidative stress markers malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) in PDLSCs after FAM30A inhibition. * P < .05 , ** P < .01 , *** P < .001 , **** P < .0001 .

Article Snippet: PDLSCs were induced for 12 hours using 100 ng/mL lipopolysaccharide from E. coli O55:B5 (LPS, HY-D1056, MCE, U.S.) to establish an in vitro cellular model.

Techniques: Concentration Assay, Knockdown, Transfection, Inhibition, Expressing

Journal: iScience

Article Title: ZDHHC17-mediated IKKβ palmitoylation suppresses NF-κB signaling to mitigate the progression of liver fibrosis

doi: 10.1016/j.isci.2026.116360

Figure Lengend Snippet: ZDHHC17 deficiency stimulates pro-inflammatory cytokines production in macrophages leading to enhanced expression of fibro-genic genes in HSCs (A) THP-1 cells were induced to M0 macrophages by PMA and further polarized to M1 macrophages by treatment with LPS/IFN-γ. ZDHHC17 was over-expressed or knocked down in M1 macrophages by plasmid transfection or siRNA. Cells were collected 48 h post-transfection for detection. LX2 cells were seeded onto the lower chamber, and M1 macrophages were plated on the upper chamber of a 0.4 μm transwell membrane, which prevents direct cell contact, limiting cell interaction to secretory chemicals. (B and C) ZDHHC17 was significantly overexpressed in M1 macrophages by plasmid transfection (B) and decreased by small interfering RNAs (siRNAs) (C). Data are presented as the mean ± SD ( n = 6 independent experiments). mRNA expression of the pro-inflammatory cytokines (TNF-α, IL-1β, and IL-12β) were detected in ZDHHC17-overexpressed (D) or ZDHHC17-silenced (E) macrophages. Data are presented as the mean ± SD ( n = 6 independent experiments). ELISA detected serum TNF-α, IL-1β, and IL-12β in ZDHHC17-overexpressed (F) or ZDHHC17-silenced (G) macrophages. Data are presented as the mean ± SD ( n = 6 independent experiments). mRNA expression of α-SMA, COL1A1, TGF-β, and TIMP-1 was detected by qPCR in LX-2 cells following co-cultured with ZDHHC17-overexpressed (H) or silenced (I) macrophages. Data were presented as mean ± SD ( n = 6 independent experiments). ∗ p < 0.05 , ∗∗ p < 0.01 , ∗∗∗ p < 0.001 , ∗∗∗∗ p < 0.0001 by Student’s t test (B-I).

Article Snippet: LPS (Lipopolysaccharide) , MCE (Monmouth Junction, NJ, USA) , Cat# HY-D1056.

Techniques: Expressing, Plasmid Preparation, Transfection, Membrane, Enzyme-linked Immunosorbent Assay, Cell Culture

Journal: Cell Reports Medicine

Article Title: Artificial exosomes synergistically reshape sepsis immune homeostasis by modulating neutrophil fate and blocking PD-1/PD-L1

doi: 10.1016/j.xcrm.2026.102819

Figure Lengend Snippet: Preparation, characterization, and interaction of AT@NV-PD1 nanoparticles with neutrophils (A) CLSM images show PD-1 (green) expression on engineered RAW 264.7 membranes (scale bars, 15 μm). (B and C) Flow cytometry quantifies PD-1 expression in primary vs. engineered cells. (D) Western blot analysis of PD-1 expression in primary and genetically engineered RAW 264.7 cells. (E and F) DLS and TEM reveal AT@NV-PD1’s hydrodynamic diameter (110–130 nm) and core-shell structure (scale bars, 50 nm). (G) CLSM demonstrates AT@NV-PD1 (red) uptake by activated neutrophils (scale bars, 10 μm). (H) Anti-PD-L1 pretreatment blocks uptake (scale bars, 10 μm). (I) Resting neutrophils show minimal uptake (scale bars, 10 μm). (J) Flow cytometry shows elevated PD-L1 on septic neutrophils. (K and L) Enhanced AT@NV-PD1 uptake in CLP-model neutrophils vs. healthy controls. (M–Q) Nanodecoys effectively neutralize inflammatory mediators (TNF-α, IL-1β, IL-6, PD-L1, LPS). All data are presented as mean ± SD ( n = 3), ∗∗ p < 0.01, ∗∗∗∗ p < 0.0001, ns, not significant.

Article Snippet: Lipopolysaccharide (LPS) , MedChemExpress (USA) , Cat. HY-D1056A1.

Techniques: Expressing, Flow Cytometry, Western Blot

Journal: Cell Reports Medicine

Article Title: Artificial exosomes synergistically reshape sepsis immune homeostasis by modulating neutrophil fate and blocking PD-1/PD-L1

doi: 10.1016/j.xcrm.2026.102819

Figure Lengend Snippet: AT@NV-PD1 regulates neutrophil fate and its mechanism in vitro (A and B) Flow cytometry analysis and quantitative results showing that AT@NV-PD1 treatment can significantly induce apoptosis in neutrophils stimulated by IFN-γ and LPS. (C) Representative immunofluorescence images of NETs; CitH3 (red), MPO (green), and DAPI (blue) staining, (scale bars, 20 μm). (D) Representative CLSM images of SYTOX Green-stained NETs. Nuclear DNA was stained with DAPI (blue), and extracellular DNA was stained with SYTOX Green (green), (scale bars, 20 μm). (E and F) Expression levels of NETs and IL-6 in neutrophils treated with different formulations, as measured by ELISA. Data are presented as mean ± standard deviation. Differences were evaluated by one-way ANOVA followed by Tukey’s multiple comparisons test, n = 5, ∗ p < 0.05, ∗∗∗ p < 0.001, ∗∗∗ p < 0.0001.

Article Snippet: Lipopolysaccharide (LPS) , MedChemExpress (USA) , Cat. HY-D1056A1.

Techniques: In Vitro, Flow Cytometry, Immunofluorescence, Staining, Expressing, Enzyme-linked Immunosorbent Assay, Standard Deviation

Journal: Cell Reports Medicine

Article Title: Artificial exosomes synergistically reshape sepsis immune homeostasis by modulating neutrophil fate and blocking PD-1/PD-L1

doi: 10.1016/j.xcrm.2026.102819

Figure Lengend Snippet: AT@NV-PD1 attenuates T cell exhaustion and promotes immune function recovery and does not impair neutrophil generation in the bone marrow (A) Flow cytometry analysis of the CD4 + /CD8 + T cell ratio in peripheral blood from CLP mice 5 days after intervention with different formulations. (B and C) Representative flow cytometry plots (B) and quantitative analysis (C) of CD4 + T cells in peripheral blood. (D and E) Representative images (D) and quantification (E) of TUNEL staining for apoptosis in splenocytes from healthy control and sepsis-treated mice (scale bars, 100 μm). (F and G) Representative flow cytometry plots (F) and quantitative analysis (G) of Treg cells in peripheral blood. (H) Flow cytometry plots of CD11b + cells in peripheral blood. (I and J) Representative flow cytometry plots and quantitative analysis of M-MDSC cells in peripheral blood. (K) Mouse body weights were monitored during the experiment, including healthy mice, PBS-treated sepsis mice, and AT@NV-PD1 -treated sepsis mice (AT7519 at a dose of 5 mg/kg). (L–O) Mice were subjected to intraperitoneal (i.p.) LPS injection to establish a sepsis model, and AT@NV-PD1 treatment was administered 4 h after LPS administration. Four hours later, LPS-challenged mice were intravenously (i.v.) injected with AT@NV-PD1 (AT7519 at a dose of 5 mg/kg). Control mice received neither LPS nor AT@NV-PD1 treatment. After 72 h, all surviving mice and control (healthy) mice were challenged with LPS (i.t. [intratracheally], 10 mg/kg). At 84 h, bronchoalveolar lavage fluid (BALF) was collected to assess neutrophil counts, IL-1β, TNF-α, and IL-6 levels. All data are presented as mean ± standard deviation (SD), and differences were evaluated by one-way ANOVA followed by Tukey’s multiple comparisons test ( n = 5; ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001).

Article Snippet: Lipopolysaccharide (LPS) , MedChemExpress (USA) , Cat. HY-D1056A1.

Techniques: Flow Cytometry, TUNEL Assay, Staining, Control, Injection, Standard Deviation