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il 8  (R&D Systems)


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    R&D Systems il 8
    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, <t>IL-8,</t> 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.
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    Images

    1) Product Images from "The cellular response capacity (CRC) as a novel immunomonitoring approach in sepsis"

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

    Journal: Military Medical Research

    doi: 10.1016/j.mmr.2026.100010

    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.
    Figure Legend 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.

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

    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.
    Figure Legend 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.

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

    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.
    Figure Legend 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.

    Techniques Used: Infection



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    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, <t>IL-8,</t> 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.
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    Image Search Results


    H1N1 infection affects cell viability, inflammatory cytokine secretion and interactions between HBEpiCs and THP-1 cells. (A) CCK-8 assay revealed that HBEpiC viability decreased in a concentration-dependent manner following H1N1 infection. (B) ELISA revealed that the levels of IL-1β, IL-6, TNF-α, and IL-8 in HBEpiCs decreased with increasing H1N1 infection. (C) CCK-8 assay indicated that supernatants from H1N1-infected HBEpiC cultures reduced the viability of THP-1 cells in a dose-dependent manner. (D) ELISA results suggested that the levels of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-8) in THP-1 cells were decreased following exposure to supernatants from H1N1-infected HBEpiC cultures. (E) Cell adhesion assay revealed that the number of THP-1 cells adhering to HBEpiCs increased with increasing H1N1 concentration (scale bar, 10 μ m). Arrow indicates THP-1 cells that remain attached to the surface of HBEpiCs, highlighting the adhesion interaction between the two cell types. (F) Transwell assay suggested that H1N1 infection enhanced the migration capacity of THP-1 cells, with increased migration observed at higher virus concentrations (scale bar, 50 μ m). The data are presented as the mean ± standard deviation; ** P<0.01, *** P<0.001 vs. control. H1N1, influenza A; HBEpiCs, human bronchial epithelial cells; ELISA, enzyme-linked immunosorbent assay; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control; MOI, multiplicity of infection.

    Journal: International Journal of Molecular Medicine

    Article Title: Triptolide exerts antiviral effects and alleviates influenza A-induced pneumonia by inhibiting the overactivation of absent in melanoma 2 signaling in immune cells

    doi: 10.3892/ijmm.2026.5829

    Figure Lengend Snippet: H1N1 infection affects cell viability, inflammatory cytokine secretion and interactions between HBEpiCs and THP-1 cells. (A) CCK-8 assay revealed that HBEpiC viability decreased in a concentration-dependent manner following H1N1 infection. (B) ELISA revealed that the levels of IL-1β, IL-6, TNF-α, and IL-8 in HBEpiCs decreased with increasing H1N1 infection. (C) CCK-8 assay indicated that supernatants from H1N1-infected HBEpiC cultures reduced the viability of THP-1 cells in a dose-dependent manner. (D) ELISA results suggested that the levels of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-8) in THP-1 cells were decreased following exposure to supernatants from H1N1-infected HBEpiC cultures. (E) Cell adhesion assay revealed that the number of THP-1 cells adhering to HBEpiCs increased with increasing H1N1 concentration (scale bar, 10 μ m). Arrow indicates THP-1 cells that remain attached to the surface of HBEpiCs, highlighting the adhesion interaction between the two cell types. (F) Transwell assay suggested that H1N1 infection enhanced the migration capacity of THP-1 cells, with increased migration observed at higher virus concentrations (scale bar, 50 μ m). The data are presented as the mean ± standard deviation; ** P<0.01, *** P<0.001 vs. control. H1N1, influenza A; HBEpiCs, human bronchial epithelial cells; ELISA, enzyme-linked immunosorbent assay; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control; MOI, multiplicity of infection.

    Article Snippet: Cell supernatants were collected and analyzed using Human TNF-α High Sensitivity ELISA Kit [cat. no. EK182HS; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.], Human IL-8 ELISA Kit [cat. no. EK108; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.], a human IL-1β ELISA kit [EH0185; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.] and IL-6 [cat. no. EK1217; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.] according to the manufacturer's instructions.

    Techniques: Infection, CCK-8 Assay, Concentration Assay, Enzyme-linked Immunosorbent Assay, Cell Adhesion Assay, Transwell Assay, Migration, Virus, Standard Deviation, Control

    TP modulates the inflammatory response and immune cell activity in H1N1-infected HBEpiCs and THP-1 cells. (A) No significant changes were observed in HBEpiCs treated with various concentrations of TP (5, 10 and 20 nM) following H1N1 infection compared with the control. (B) After TP treatment, the levels of the inflammatory cytokines IL-1β, IL-6, TNF-α and IL-8 in HBEpiCs were markedly lower than those in the untreated group. (C) The viability of THP-1 cells pretreated with H1N1-infected HBEpiC culture supernatant decreased after TP treatment. (D) The levels of IL-1β, IL-6, TNF-α, and IL-8 in THP-1 cells were markedly lower after TP treatment. (E) The adhesion of THP-1 cells to HBEpiCs induced by H1N1 infection decreased in a dose-dependent manner with increasing TP concentration (scale bar, 10 μ m). Arrow indicates THP-1 cells that remain attached to the surface of HBEpiCs, highlighting the adhesion interaction between the two cell types. (F) The migration capacity of THP-1 cells was markedly reduced when the supernatant from H1N1-infected HBEpiC cultures was treated with TP (scale bar, 50 μ m). The data are presented as the mean ± standard deviation; * P<0.05, ** P<0.01, *** P<0.001 vs. control. TP, triptolide; H1N1, influenza A; HBEpiCs, human bronchial epithelial cells; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control.

    Journal: International Journal of Molecular Medicine

    Article Title: Triptolide exerts antiviral effects and alleviates influenza A-induced pneumonia by inhibiting the overactivation of absent in melanoma 2 signaling in immune cells

    doi: 10.3892/ijmm.2026.5829

    Figure Lengend Snippet: TP modulates the inflammatory response and immune cell activity in H1N1-infected HBEpiCs and THP-1 cells. (A) No significant changes were observed in HBEpiCs treated with various concentrations of TP (5, 10 and 20 nM) following H1N1 infection compared with the control. (B) After TP treatment, the levels of the inflammatory cytokines IL-1β, IL-6, TNF-α and IL-8 in HBEpiCs were markedly lower than those in the untreated group. (C) The viability of THP-1 cells pretreated with H1N1-infected HBEpiC culture supernatant decreased after TP treatment. (D) The levels of IL-1β, IL-6, TNF-α, and IL-8 in THP-1 cells were markedly lower after TP treatment. (E) The adhesion of THP-1 cells to HBEpiCs induced by H1N1 infection decreased in a dose-dependent manner with increasing TP concentration (scale bar, 10 μ m). Arrow indicates THP-1 cells that remain attached to the surface of HBEpiCs, highlighting the adhesion interaction between the two cell types. (F) The migration capacity of THP-1 cells was markedly reduced when the supernatant from H1N1-infected HBEpiC cultures was treated with TP (scale bar, 50 μ m). The data are presented as the mean ± standard deviation; * P<0.05, ** P<0.01, *** P<0.001 vs. control. TP, triptolide; H1N1, influenza A; HBEpiCs, human bronchial epithelial cells; IL, interleukin; TNF-α, tumor necrosis factor-α; Con, control.

    Article Snippet: Cell supernatants were collected and analyzed using Human TNF-α High Sensitivity ELISA Kit [cat. no. EK182HS; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.], Human IL-8 ELISA Kit [cat. no. EK108; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.], a human IL-1β ELISA kit [EH0185; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.] and IL-6 [cat. no. EK1217; Hangzhou Multi Sciences (Lianke) Biotech Co., Ltd.] according to the manufacturer's instructions.

    Techniques: Activity Assay, Infection, Control, Concentration Assay, Migration, Standard Deviation

    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.

    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

    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.

    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

    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.

    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

    Preventative efficacy of DTI@EcN against DSS-induced colitis. ( A ) Schematic of the experimental schedule. Mice received daily oral gavage of various bacterial formulations or drugs throughout the experimental period (bacteria: 5 × 10 8 CFU; IDE: 65 mg/kg). 3% DSS was given via drinking water from day 4 to day 8 to induce colitis. ( B ) Quantitative assessment of body weight variation in colitis mice across treatment groups. ( C ) Macroscopic appearance of colon tissues and ( D ) corresponding length measurements. ( E ) Histopathological evaluation by H&E staining and ( F ) histopathological scores of colon tissues based on H&E images. Scale bar: 100 μm. ( G ) Immunofluorescence localization of tight junction proteins ZO-1 (red) and Occludin (green) in colonic epithelia. Cell nuclei were stained with DAPI (blue). Scale bar: 100 μm. ( H ) Quantified ZO-1 and ( I ) occludin fluorescence intensities in colon tissues shown in (G) through ImageJ. ( J ) LSCM images showing DCF fluorescence in colon tissues incubated with DCFH-DA, representing the relative ROS levels across different treatment groups. Scale bar: 100 μm. ( K ) Quantified DCF fluorescence intensities from (J), analyzed with ImageJ. ( L ) Relative colonic MPO activities in colon tissues in different treatment groups. ( M - P ) Levels of pro-inflammatory cytokines, including IL-6 ( M ), IL-1β ( N ), TNF-α (O), and IFN-γ ( P ), in colon tissues, determined by ELISA kits. Data represent the mean ± SEM (n = 5). Statistical analysis was performed using one-way ANOVA. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Journal: Materials Today Bio

    Article Title: Prodrug-integrated multifunctional liposome encapsulation enhances probiotic-based bacteriotherapy for inflammatory bowel disease

    doi: 10.1016/j.mtbio.2026.103110

    Figure Lengend Snippet: Preventative efficacy of DTI@EcN against DSS-induced colitis. ( A ) Schematic of the experimental schedule. Mice received daily oral gavage of various bacterial formulations or drugs throughout the experimental period (bacteria: 5 × 10 8 CFU; IDE: 65 mg/kg). 3% DSS was given via drinking water from day 4 to day 8 to induce colitis. ( B ) Quantitative assessment of body weight variation in colitis mice across treatment groups. ( C ) Macroscopic appearance of colon tissues and ( D ) corresponding length measurements. ( E ) Histopathological evaluation by H&E staining and ( F ) histopathological scores of colon tissues based on H&E images. Scale bar: 100 μm. ( G ) Immunofluorescence localization of tight junction proteins ZO-1 (red) and Occludin (green) in colonic epithelia. Cell nuclei were stained with DAPI (blue). Scale bar: 100 μm. ( H ) Quantified ZO-1 and ( I ) occludin fluorescence intensities in colon tissues shown in (G) through ImageJ. ( J ) LSCM images showing DCF fluorescence in colon tissues incubated with DCFH-DA, representing the relative ROS levels across different treatment groups. Scale bar: 100 μm. ( K ) Quantified DCF fluorescence intensities from (J), analyzed with ImageJ. ( L ) Relative colonic MPO activities in colon tissues in different treatment groups. ( M - P ) Levels of pro-inflammatory cytokines, including IL-6 ( M ), IL-1β ( N ), TNF-α (O), and IFN-γ ( P ), in colon tissues, determined by ELISA kits. Data represent the mean ± SEM (n = 5). Statistical analysis was performed using one-way ANOVA. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Article Snippet: The selected chemicals and biological materials used in this research are as follows: 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide (EDCI, Macklin), 4-bromobutyric acid (Bidepharm), thiourea (Macklin), sodium hydroxide (NaOH, Macklin), hydrochloric acid (HCl, Macklin), trifluoroacetic acid (Bidepharm), idebenone (Bidepharm), hexadecyltrimethylammonium bromide (Macklin), 4-dimethylaminopyridine (DMAP, Macklin), N-hydroxysuccinimide (NHS, Macklin), 2′,7′-dichlorofluorescin diacetate (DCFH-DA, Aladdin), DSPE-PEG2000-NH 2 (Yusi), DSPE-PEG2000-FITC (Yusi), cholesterol (Yuanye), trypsin (Macklin), pepsin powder (Bidepharm), bile salts (Macklin), ampicillin (Bidepharm), lysin (Bidepharm), dextran sulfate sodium salt (DSS, MW 40,000, MP Bio), LB nutrient agar (Hopebiol), Cell Counting Kit-8 (CCK-8, Beyotime), mouse IL-6, IFN-γ, IL-1β, and TNF-α uncoated ELISA kits (Thermo Fisher Scientific), and antigen retrieval solution (Servicebio).

    Techniques: Bacteria, Staining, Immunofluorescence, Fluorescence, Incubation, Enzyme-linked Immunosorbent Assay

    Therapeutic efficacy of DTI@EcN against DSS-induced colitis. ( A ) Schematic of the experimental schedule. Colitis was induced by administering 3% DSS in drinking water for the first 5 days. Subsequently, different treatments were administered daily for 5 days to evaluate their therapeutic efficacy. ( B ) Body weight dynamics of colitis mice under different treatments. ( C ) Macroscopic colon appearance and ( D ) corresponding length measurements across groups. ( E) Histopathological assessment by H&E staining. Scale bar: 100 μm. ( F ) Histopathology scores of colon tissues based on the H&E images. ( G ) Localization of tight junction proteins ZO-1 (red) and occludin (green) in colonic epithelium across treatment groups. Cell nuclei were stained with DAPI (blue). Scale bar: 100 μm. ( H ) Quantification of ZO-1 and ( I ) Occludin fluorescence intensities from (G), analyzed using ImageJ. ( J ) LSCM images showing DCF fluorescence in colon tissues incubated with DCFH-DA, representing the relative ROS levels across different treatment groups. Scale bar: 100 μm. ( K ) Quantitative analysis of DCF fluorescence intensities from (J). ( L ) Relative MPO activity in colon tissues across various treatment groups. ( M - P ) Levels of pro-inflammatory cytokines, including IL-6 ( M ), IL-1β ( N ), TNF-α ( O ), and IFN-γ ( P ), in colon tissues, measured by ELISA kits. Data represented the mean ± SEM (n = 5 or 6). Statistical analysis was performed using one-way ANOVA. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Journal: Materials Today Bio

    Article Title: Prodrug-integrated multifunctional liposome encapsulation enhances probiotic-based bacteriotherapy for inflammatory bowel disease

    doi: 10.1016/j.mtbio.2026.103110

    Figure Lengend Snippet: Therapeutic efficacy of DTI@EcN against DSS-induced colitis. ( A ) Schematic of the experimental schedule. Colitis was induced by administering 3% DSS in drinking water for the first 5 days. Subsequently, different treatments were administered daily for 5 days to evaluate their therapeutic efficacy. ( B ) Body weight dynamics of colitis mice under different treatments. ( C ) Macroscopic colon appearance and ( D ) corresponding length measurements across groups. ( E) Histopathological assessment by H&E staining. Scale bar: 100 μm. ( F ) Histopathology scores of colon tissues based on the H&E images. ( G ) Localization of tight junction proteins ZO-1 (red) and occludin (green) in colonic epithelium across treatment groups. Cell nuclei were stained with DAPI (blue). Scale bar: 100 μm. ( H ) Quantification of ZO-1 and ( I ) Occludin fluorescence intensities from (G), analyzed using ImageJ. ( J ) LSCM images showing DCF fluorescence in colon tissues incubated with DCFH-DA, representing the relative ROS levels across different treatment groups. Scale bar: 100 μm. ( K ) Quantitative analysis of DCF fluorescence intensities from (J). ( L ) Relative MPO activity in colon tissues across various treatment groups. ( M - P ) Levels of pro-inflammatory cytokines, including IL-6 ( M ), IL-1β ( N ), TNF-α ( O ), and IFN-γ ( P ), in colon tissues, measured by ELISA kits. Data represented the mean ± SEM (n = 5 or 6). Statistical analysis was performed using one-way ANOVA. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

    Article Snippet: The selected chemicals and biological materials used in this research are as follows: 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide (EDCI, Macklin), 4-bromobutyric acid (Bidepharm), thiourea (Macklin), sodium hydroxide (NaOH, Macklin), hydrochloric acid (HCl, Macklin), trifluoroacetic acid (Bidepharm), idebenone (Bidepharm), hexadecyltrimethylammonium bromide (Macklin), 4-dimethylaminopyridine (DMAP, Macklin), N-hydroxysuccinimide (NHS, Macklin), 2′,7′-dichlorofluorescin diacetate (DCFH-DA, Aladdin), DSPE-PEG2000-NH 2 (Yusi), DSPE-PEG2000-FITC (Yusi), cholesterol (Yuanye), trypsin (Macklin), pepsin powder (Bidepharm), bile salts (Macklin), ampicillin (Bidepharm), lysin (Bidepharm), dextran sulfate sodium salt (DSS, MW 40,000, MP Bio), LB nutrient agar (Hopebiol), Cell Counting Kit-8 (CCK-8, Beyotime), mouse IL-6, IFN-γ, IL-1β, and TNF-α uncoated ELISA kits (Thermo Fisher Scientific), and antigen retrieval solution (Servicebio).

    Techniques: Drug discovery, Staining, Histopathology, Fluorescence, Incubation, Activity Assay, Enzyme-linked Immunosorbent Assay

    Therapeutic efficacy of DTI@EcN against STm-induced colitis. ( A ) Schematic of the experimental schedule. C57BL/6J mice were pretreated with streptomycin (100 μL, 200 mg/mL) one day prior to oral administration with STm. Afterward, different bacterial formulations were given to mice for 4 days to evaluate their effectiveness against STm-induced colitis. ( B ) Changes in STm counts in feces during the treatment period. ( C ) Quantification of STm per mg of feces on day 4 post-administration of various EcN formulations. ( D ) STm and ( E ) EcN counts in the cecum after different treatments. ( F ) Histological evaluation of colon damage with H&E staining (Scale bar: 100 μm) and ( G ) corresponding histopathology scores, respectively. ( H ) Neutrophil infiltration measured by colonic MPO activity. ( I - L ) Levels of pro-inflammatory cytokines in colon tissues, including IL-6 ( I ), IL-1β ( J ), TNF-α ( K ), and IFN-γ ( L ), as determined by ELISA kits. Data are presented as means ± SEM (n = 5). Statistical analysis was performed using one-way ANOVA. ns: no significance, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

    Journal: Materials Today Bio

    Article Title: Prodrug-integrated multifunctional liposome encapsulation enhances probiotic-based bacteriotherapy for inflammatory bowel disease

    doi: 10.1016/j.mtbio.2026.103110

    Figure Lengend Snippet: Therapeutic efficacy of DTI@EcN against STm-induced colitis. ( A ) Schematic of the experimental schedule. C57BL/6J mice were pretreated with streptomycin (100 μL, 200 mg/mL) one day prior to oral administration with STm. Afterward, different bacterial formulations were given to mice for 4 days to evaluate their effectiveness against STm-induced colitis. ( B ) Changes in STm counts in feces during the treatment period. ( C ) Quantification of STm per mg of feces on day 4 post-administration of various EcN formulations. ( D ) STm and ( E ) EcN counts in the cecum after different treatments. ( F ) Histological evaluation of colon damage with H&E staining (Scale bar: 100 μm) and ( G ) corresponding histopathology scores, respectively. ( H ) Neutrophil infiltration measured by colonic MPO activity. ( I - L ) Levels of pro-inflammatory cytokines in colon tissues, including IL-6 ( I ), IL-1β ( J ), TNF-α ( K ), and IFN-γ ( L ), as determined by ELISA kits. Data are presented as means ± SEM (n = 5). Statistical analysis was performed using one-way ANOVA. ns: no significance, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

    Article Snippet: The selected chemicals and biological materials used in this research are as follows: 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide (EDCI, Macklin), 4-bromobutyric acid (Bidepharm), thiourea (Macklin), sodium hydroxide (NaOH, Macklin), hydrochloric acid (HCl, Macklin), trifluoroacetic acid (Bidepharm), idebenone (Bidepharm), hexadecyltrimethylammonium bromide (Macklin), 4-dimethylaminopyridine (DMAP, Macklin), N-hydroxysuccinimide (NHS, Macklin), 2′,7′-dichlorofluorescin diacetate (DCFH-DA, Aladdin), DSPE-PEG2000-NH 2 (Yusi), DSPE-PEG2000-FITC (Yusi), cholesterol (Yuanye), trypsin (Macklin), pepsin powder (Bidepharm), bile salts (Macklin), ampicillin (Bidepharm), lysin (Bidepharm), dextran sulfate sodium salt (DSS, MW 40,000, MP Bio), LB nutrient agar (Hopebiol), Cell Counting Kit-8 (CCK-8, Beyotime), mouse IL-6, IFN-γ, IL-1β, and TNF-α uncoated ELISA kits (Thermo Fisher Scientific), and antigen retrieval solution (Servicebio).

    Techniques: Drug discovery, Staining, Histopathology, Activity Assay, Enzyme-linked Immunosorbent Assay