Journal: JHEP Reports

Article Title: Myeloid TGF-β signaling shapes liver macrophage heterogeneity and metabolic liver disease pathogenesis

doi: 10.1016/j.jhepr.2025.101488

Figure Lengend Snippet: Tgfbr1 ablation triggers the induction of proinflammatory and senescent macrophages in liver. (A) Feature plots illustrating Pycard, Casp1, Nlrp3, and Il1b mRNA expression within macrophage subclusters. (B) qPCR analysis of gene expression in cultured liver macrophages isolated from control and MKO MASH livers treated with PBS (n = 3) or LPS (5 ng/ml) plus IFN-γ (5 ng/ml) (n = 3). (C) Immunoblots of total protein lysates from cultured liver macrophages. Primary macrophages isolated from control and MKO mouse livers were treated with PBS (n = 2) or LPS (200 ng/ml) (n = 2) for 3 h followed by ATP (3 mM) treatment for 30 min. (D) Cytokine concentrations in conditioned media from cultured liver macrophages treated with PBS (n = 4) or LPS (200 ng/ml) (n = 4) for 3 h followed by ATP (3 mM) stimulation for 30 min. Data in (B and D) represent mean ± SEM; analyzed by one-way ANOVA with post hoc analysis using Tukey’s test. IFN-γ, interferon-γ; LPS, lipopolysaccharide; MKO, myeloid-specific knockout; MASH, metabolic dysfunction-associated steatohepatitis; qPCR, quantitative PCR.

Article Snippet: Antibodies against IL-1β, cleaved IL-1β, caspase 1, cleaved caspase 1, and NLRP3 (contained in a mouse reactive inflammasome antibody sampler kit; catalog #20836), as well as p16 INK4A and p21 Waf1/Cip1 (contained in Senescence Marker Antibody Sampler Kit; catalog #56062) were purchased from Cell Signaling Technology.

Techniques: Expressing, Gene Expression, Cell Culture, Isolation, Control, Western Blot, Knock-Out, Real-time Polymerase Chain Reaction

Journal: ImmunoTargets and Therapy

Article Title: Recombinant Antithrombin Alleviated Pulmonary Injury and Inflammation in LPS-Induced ARDS by Inhibiting IL17a/NF-κB Signaling

doi: 10.2147/ITT.S502925

Figure Lengend Snippet: rAT reduced pulmonary inflammation in LPS-induced ARDS model mice. ( A–D ) The levels of inflammatory factors, including IL-6 ( A ), TNF-α ( B ), IL-8 ( C ), and hs-CRP ( D ), were decreased in the serum of the rAT-treated group, as detected by ELISA. ( E ) Immunohistochemical staining for F4/80 revealed that rAT treatment reduced the proportion of macrophages in the lung tissue of LPS-induced ARDS model mice. ( F ) Immunohistochemical staining for MRCI, a marker of M2 macrophages, showed that rAT treatment increased the proportion of M2 macrophages in the lung tissue of LPS-induced ARDS model mice. ( G ) Immunohistochemical staining for Ly6G, a marker of neutrophils, showed that rAT treatment reduced the proportion of neutrophils in the lung tissue of LPS-induced ARDS model mice. All the data are presented as the means ± SDs of three independent experiments. One-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001, ns, not significant; scale bar, 50 μm.

Article Snippet: A mouse CXCL15 ELISA Kit (E-EL-M0269) and a mouse hs-CRP ELISA Kit (E-EL-M0677) were purchased from Elabscience (Wuhan, China).

Techniques: Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Staining, Marker

Journal: ImmunoTargets and Therapy

Article Title: Recombinant Antithrombin Alleviated Pulmonary Injury and Inflammation in LPS-Induced ARDS by Inhibiting IL17a/NF-κB Signaling

doi: 10.2147/ITT.S502925

Figure Lengend Snippet: The efficacy of rAT in mitigating lung injury, suppressing the immune response, and inhibiting the activation of the NF-κB signaling pathway in LPS-induced ARDS mice were diminished by the administration of IL-17a. ( A ) ELISA results demonstrated that the administration of IL17a inhibited the ability of rAT to reduce inflammatory factors, including IL-6, TNF-α, and IL-8, in the serum of LPS-induced ARDS mice. ( B ) The analysis of the wet/dry weight ratio of the lung tissue revealed that the administration of IL17a counteracted the ability of rAT to alleviate pulmonary exudation in LPS-induced ARDS mice. ( C ) The administration of IL17a did not significantly affect the ability of rAT to reduce the number of cells in the BALF of LPS-induced ARDS mice. ( D ) The administration of IL17a attenuated the ability of rAT to reduce the concentrations of proteins in the BALF of LPS-induced ARDS mice. ( E ) Real-time PCR results showed that the administration of IL17a blocked the ability of rAT to downregulate the expression of target genes in the IL17a/NF-κB signaling pathway. ( F ) The protein levels of the NF-κB signaling pathway were assessed by Western blotting, and gray intensity analysis of the blots showed that the administration of IL17a in LPS-induced ARDS mice counteracted the ability of rAT to suppress the phosphorylation of IκBα, IKKα/β, and P65. The data are expressed as the means ± SDs (n=3 in each group). One-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001, and ns not significant.

Article Snippet: A mouse CXCL15 ELISA Kit (E-EL-M0269) and a mouse hs-CRP ELISA Kit (E-EL-M0677) were purchased from Elabscience (Wuhan, China).

Techniques: Activation Assay, Enzyme-linked Immunosorbent Assay, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Phospho-proteomics