Journal: Regenerative Therapy

Article Title: Prednisolone attenuates the immunomodulatory capacity and reshapes the functional phenotype of canine adipose-derived mesenchymal stromal cells

doi: 10.1016/j.reth.2026.101184

Figure Lengend Snippet: Effects of prednisolone on macrophage polarization and regulatory T (Treg) cell induction mediated by cADSCs. (a) Representative flow cytometry plots showing cluster designation (CD) 80 and CD206 expression in CD14 + DH82 cells. Cells cultured alone under control conditions or stimulated with interleukin (IL)-4/IL-13 or lipopolysaccharide (LPS)/interferon (IFN)-γ are shown, together with DH82 cells co-cultured with cADSCs pretreated with prednisolone at the indicated concentrations (0–100 μM) under LPS/IFN-γ stimulation. (b) Quantitative analysis of macrophage subsets, defined as CD14 + CD80 + CD206 - , CD14 + CD80 − CD206 + , CD14 + CD80 + CD206 + , and CD14 + CD80 − CD206 - cells. IL-4/IL-13 stimulation was included as an M2-polarizing control, whereas LPS/IFN-γ stimulation induced M1-like polarization. (c) Representative flow cytometry plots showing CD25 and Foxp3 expression in CD4 + T cells after co-culture of PBMCs with cADSCs pretreated with prednisolone. Red boxes indicate CD25 + Foxp3 + Treg cells. (d) Quantification of CD25 + Foxp3 + Treg cells within the CD4 + T-cell population. Data are presented as mean ± SD from three independent experiments using cADSCs derived from three independent donors. * p < 0.05 vs. control or PBMCs alone; † p < 0.05 vs. LPS/IFN-γ.

Article Snippet: To induce macrophage polarization, either a combination of 50 ng/mL lipopolysaccharide (LPS; Sigma-Aldrich) and 20 ng/mL recombinant canine interferon (IFN)-γ (R&D Systems), or a combination of 40 ng/mL recombinant human interleukin (IL)-4 (Thermo Fisher Scientific) and 40 ng/mL recombinant human IL-13 (Thermo Fisher Scientific), was added to the cultures, followed by incubation at 37 °C in 5% CO 2 for 72 h. At the end of the co-culture period, cells were collected, washed with FACS buffer, and incubated on ice with canine Fc receptor binding inhibitor.

Techniques: Flow Cytometry, Expressing, Cell Culture, Control, Analysis, Co-culture Assay, Derivative Assay

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Concentration-dependent change in the humoral inflammatory response following incubation with Escherichia coli ( E. coli ) in the ex vivo whole blood model. a Absolute plasma concentrations of IL-6, IL-8, and MMP9 determined by enzyme-linked immunosorbent assay. b Normalized values and EC 50 curve fit by BuC=0% and 50 000 CFU/ml E. coli= 100%, respectively, for IL-6, IL-8, and MMP9 as indicated by EC 50 (%) on the respective Y-axis. BuC indicates buffer control after 60 min incubation; numbers on the X-axis indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation; LPS indicates lipopolysaccharide (LPS) 100 ng/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, comparing all shown concentrations of E. coli bacteria and 100 ng/ml LPS with BuC. P -values are indicated above the respective data points. ⁎ P <0.05, ⁎⁎ P <0.01, ⁎⁎⁎ P <0.001. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Concentration Assay, Incubation, Ex Vivo, Clinical Proteomics, Enzyme-linked Immunosorbent Assay, Control, Bacteria

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Diagnostic performance for the detection of bacteremia, analyzing the neutrophil phenotype by determining the median fluorescence intensity (MFI) and the cellular response capacity (CRC) in comparison with traditional markers of humoral inflammation (IL-6, IL-8, MMP9). a Comparison of receiver operating characteristic (ROC) at 10,000 CFU/ml Escherichia coli ( E. coli ) with the respective 95% confidence interval (CI) and P -value, and half-maximal effective concentration (EC 50 ) as a function of the E. coli concentration. b Detailed comparison of the EC 50 as a function of the E. coli concentration. c Exemplary comparison of EC 50 curve fit after normalization as indicated by EC 50 (%) on the respective Y-axis to BuC=100% and 50 000 CFU/ml E. coli =0% for the humoral marker IL-6 (the IL-6 values were multiplied by −1 before EC 50 calculation to facilitate comparability with the CRC) and the change in neutrophil phenotype represented by CD11b CRC. BuC indicates buffer control after 60 min incubation; numbers on the X-axis of c indicate E. coli bacteria in concentrations of 2000 to 50 000 CFU/ml after 60 min incubation. Values are shown as median and interquartile range. n =8. Statistical analysis was performed using the Kruskal-Wallis test with Dunn’s post-hoc test, evaluating the EC 50 of IL-8, MMP9, the MFI, and CRC of CD10, CD11b, and CD62L in comparison to the EC 50 of IL-6. P -values are indicated above the respective data points. ⁎ P <0.05. CFU. Colony-forming units; IL. Interleukin; MMP9. Matrix metallopeptidase 9.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Diagnostic Assay, Fluorescence, Comparison, Concentration Assay, Marker, Control, Incubation, Bacteria

Journal: Military Medical Research

Article Title: The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis

doi: 10.1016/j.mmr.2026.100010

Figure Lengend Snippet: Clinical specifications and parameters over all time points of the sepsis cohort. a Suspected infection cause of sepsis. b Distribution of the individual score points of the Sequential Organ Failure Assessment (SOFA) score. c Total SOFA score. d-h Traditional and humoral markers of inflammation: leukocytes and neutrophil-lymphocyte ratio ( d ), C-reactive protein (CRP) and procalcitonin (PCT) ( e ), interleukin-6 (IL-6) and interleukin-8 (IL-8) ( f ), serum amyloid A (SAA) and calprotectin ( g ), matrix metallopeptidase 9 (MMP9) and myeloperoxidase (MPO) ( h ). Values are shown as median and interquartile range. n =14. CNS. Central nervous system; HV. Healthy volunteers.

Article Snippet: For the samples of the ex vivo whole blood model, the plasma concentrations of matrix metallopeptidase 9 (MMP9, #DY911, R&D Systems, Minneapolis, USA), IL-6 (#555220, BD Biosciences, San Jose, USA), and IL-8 (#DY208, R&D Systems) were measured in citrate-anticoagulated plasma using enzyme-linked immunosorbent assay according to the respective manufacturer’s instructions.

Techniques: Infection

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet: Schematic illustration of the role of SUR1 in ALI and the protective mechanism of glibenclamide TNF-α binds to its receptor (TNFR), activating the NF-κB pathway and promoting inflammation through increased transcription of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α). In parallel, TNF-α induces mitochondrial dysfunction and ROS production, leading to DNA strand breaks. In response to DNA damage, nuclear PARP1 is activated to recruit DNA repair enzymes, promoting cell survival. Left, SUR1 interacts with and sequesters PARP1, impairing DNA damage repair. Accumulated DNA damage amplifies ROS production and NF-κB activation, which in turn further increases the transcription of inflammatory cytokines. This creates a positive feedback loop that promotes epithelial cell apoptosis and inflammation, contributing to ALI progression. Right, glibenclamide binds to SUR1 and disrupts the SUR1-PARP1 interaction, releasing PARP1 to restore DNA damage repair. This intervention breaks the pathological feedback loop by reducing ROS production, NF-κB activation, and inflammatory cytokine expression, thereby suppressing apoptosis and inflammation in epithelial cells and ultimately protecting against ALI.

Article Snippet: Recombinant human IL-6 protein , ABclonal Biotechnology , Cat# RP00201.

Techniques: Activation Assay, Expressing

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet:

Article Snippet: Recombinant human IL-6 protein , ABclonal Biotechnology , Cat# RP00201.

Techniques: Cell-Signaling, Recombinant, Transfection, Caspase-3 Activity Assay, Protein Extraction, Knock-Out, Sequencing, Control, Plasmid Preparation, Software, Analysis