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Fig. 1. PVL induces ROS-independent NET formation. (A, B) ROS formation was quantified in control (A: n = 14, B: n = 3) or CGD human (n = 3) primary <t>neutrophils</t> stimulated with PMA (50 nM) or PVL (0.1 nM, 1 nM or 10 nM). (C) Control or CGD neutrophils were stimulated with PMA (50 nM) or PVL (10 nM) for 3 h, and cell death was quantified using the cell-impermeable DNA dye SYTOX Green. Indicated is SYTOX Green fluorescence relative to t = 0 min. (D) Representative confocal microscopy images of control and CGD patient neutrophils either naïve or stimulated with PMA (50 nM) or PVL (1 nM or 10 nM) and stained for DNA (blue), NE (red), and chromatin (green). The scale bar represents 10 µm. (E–G) Healthy human neutrophils were treated with PKC inhibitor Gö6983 (1 μM), BAPTA-AM (10 μM), DPI (1 μM), pyrocatechol (30 μM), ABAH (500 μM), NEi (20 μM), and AEBSF (100 μM) for 30 min, before stimulating with (E) PVL 1 nM, (F) PVL 10 nM, or (G) PMA 50 nM for 4 h. We quantified cell death with SYTOX Green and the fluorescence signal relative to naïve is indicated. (H) Representative confocal microscopy of naïve neutrophils or after stimulation with PMA or PVL (1 nM or 10 nM) in the presence or absence of indicated inhibitors, and stained for DNA (blue), NE (red), and chromatin (green). The scale bar represents 10 µm. (C) Two-way analysis of variance with Tukey’s post hoc test. *P < 0.05, ***P < 0.001. (E–G) Mean ± SD of 4 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, 1-way analysis of variance with Dunnett’s multiple comparison test. ns = not significant.

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1) Product Images from "Panton-Valentine leukocidin-induced neutrophil extracellular traps lack antimicrobial activity and are readily induced in patients with recurrent PVL+-Staphylococcus aureus infections."

Article Title: Panton-Valentine leukocidin-induced neutrophil extracellular traps lack antimicrobial activity and are readily induced in patients with recurrent PVL+-Staphylococcus aureus infections.

Journal: Journal of leukocyte biology

doi: 10.1093/jleuko/qiad137

Fig. 1. PVL induces ROS-independent NET formation. (A, B) ROS formation was quantified in control (A: n = 14, B: n = 3) or CGD human (n = 3) primary neutrophils stimulated with PMA (50 nM) or PVL (0.1 nM, 1 nM or 10 nM). (C) Control or CGD neutrophils were stimulated with PMA (50 nM) or PVL (10 nM) for 3 h, and cell death was quantified using the cell-impermeable DNA dye SYTOX Green. Indicated is SYTOX Green fluorescence relative to t = 0 min. (D) Representative confocal microscopy images of control and CGD patient neutrophils either naïve or stimulated with PMA (50 nM) or PVL (1 nM or 10 nM) and stained for DNA (blue), NE (red), and chromatin (green). The scale bar represents 10 µm. (E–G) Healthy human neutrophils were treated with PKC inhibitor Gö6983 (1 μM), BAPTA-AM (10 μM), DPI (1 μM), pyrocatechol (30 μM), ABAH (500 μM), NEi (20 μM), and AEBSF (100 μM) for 30 min, before stimulating with (E) PVL 1 nM, (F) PVL 10 nM, or (G) PMA 50 nM for 4 h. We quantified cell death with SYTOX Green and the fluorescence signal relative to naïve is indicated. (H) Representative confocal microscopy of naïve neutrophils or after stimulation with PMA or PVL (1 nM or 10 nM) in the presence or absence of indicated inhibitors, and stained for DNA (blue), NE (red), and chromatin (green). The scale bar represents 10 µm. (C) Two-way analysis of variance with Tukey’s post hoc test. *P < 0.05, ***P < 0.001. (E–G) Mean ± SD of 4 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, 1-way analysis of variance with Dunnett’s multiple comparison test. ns = not significant.

Figure Legend Snippet: Fig. 1. PVL induces ROS-independent NET formation. (A, B) ROS formation was quantified in control (A: n = 14, B: n = 3) or CGD human (n = 3) primary neutrophils stimulated with PMA (50 nM) or PVL (0.1 nM, 1 nM or 10 nM). (C) Control or CGD neutrophils were stimulated with PMA (50 nM) or PVL (10 nM) for 3 h, and cell death was quantified using the cell-impermeable DNA dye SYTOX Green. Indicated is SYTOX Green fluorescence relative to t = 0 min. (D) Representative confocal microscopy images of control and CGD patient neutrophils either naïve or stimulated with PMA (50 nM) or PVL (1 nM or 10 nM) and stained for DNA (blue), NE (red), and chromatin (green). The scale bar represents 10 µm. (E–G) Healthy human neutrophils were treated with PKC inhibitor Gö6983 (1 μM), BAPTA-AM (10 μM), DPI (1 μM), pyrocatechol (30 μM), ABAH (500 μM), NEi (20 μM), and AEBSF (100 μM) for 30 min, before stimulating with (E) PVL 1 nM, (F) PVL 10 nM, or (G) PMA 50 nM for 4 h. We quantified cell death with SYTOX Green and the fluorescence signal relative to naïve is indicated. (H) Representative confocal microscopy of naïve neutrophils or after stimulation with PMA or PVL (1 nM or 10 nM) in the presence or absence of indicated inhibitors, and stained for DNA (blue), NE (red), and chromatin (green). The scale bar represents 10 µm. (C) Two-way analysis of variance with Tukey’s post hoc test. *P < 0.05, ***P < 0.001. (E–G) Mean ± SD of 4 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, 1-way analysis of variance with Dunnett’s multiple comparison test. ns = not significant.

Techniques Used: Control, Fluorescence, Confocal Microscopy, Staining, Comparison

Fig. 2. NET proteome assembly is different in PVL-induced NETs. (A) Principal component analysis of the proteomes of naïve neutrophils, and PVL-induced (10 nM), PMA-induced (50 nM), and nigericin-induced (15 µM) NETs. Analysis was performed on scaled log2-abundance of all proteins detected in at least 2 of 3 replicates. (B) Euler diagram showing the number and distribution of significant differentially abundant peptides (logFC > 1, adjusted P < 0.01) on NETs compared with naïve neutrophils. Areas are proportional to DAP set size. (C) Clustered heatmap showing fold change (log2) values on each NET sample compared with naïve neutrophils of significant DAPs from panel B. Clustering was performed by k-means algorithm with k = 4 clusters. (D, E) Top 25 most abundant DAPs that are significantly differentially abundant on PVL-induced NETs compared with PMA-induced (D) and nigericin-induced NETs (E). Point size and fill color represent average abundance across samples and adjusted P value, respectively. Proteomes were made from n = 3 samples per condition from independent donors. DAP significance for each comparison was determined by a threshold of |[log2 fold change]| > 1 and adjusted P value < 0.01.

Figure Legend Snippet: Fig. 2. NET proteome assembly is different in PVL-induced NETs. (A) Principal component analysis of the proteomes of naïve neutrophils, and PVL-induced (10 nM), PMA-induced (50 nM), and nigericin-induced (15 µM) NETs. Analysis was performed on scaled log2-abundance of all proteins detected in at least 2 of 3 replicates. (B) Euler diagram showing the number and distribution of significant differentially abundant peptides (logFC > 1, adjusted P < 0.01) on NETs compared with naïve neutrophils. Areas are proportional to DAP set size. (C) Clustered heatmap showing fold change (log2) values on each NET sample compared with naïve neutrophils of significant DAPs from panel B. Clustering was performed by k-means algorithm with k = 4 clusters. (D, E) Top 25 most abundant DAPs that are significantly differentially abundant on PVL-induced NETs compared with PMA-induced (D) and nigericin-induced NETs (E). Point size and fill color represent average abundance across samples and adjusted P value, respectively. Proteomes were made from n = 3 samples per condition from independent donors. DAP significance for each comparison was determined by a threshold of |[log2 fold change]| > 1 and adjusted P value < 0.01.

Techniques Used: Comparison

Fig. 3. PVL-induced NETs do not kill MRSA. (A) Primary human neutrophils were stimulated with PVL (100 nM), PMA (100 nM), or nigericin (30 µM) for 4 h to induce NETs. MRSA was incubated with these NETs for 1 h and colony-forming units was quantified after overnight incubation on TSA plates. Bacterial viability is expressed as a percentage of colony-forming units normalized to MRSA incubated in the absence of NETs. (B) The DNA content of PVL-, PMA-, and nigericin-induced NETs at 4 h was quantified by spectrophotometry. (A) Mean ± SD of 5 independent experiments. *P < 0.05, *** P < 0.001, 1-way analysis of variance. (B) Mean ± SD of 4 independent experiments. ns = not significant.

Figure Legend Snippet: Fig. 3. PVL-induced NETs do not kill MRSA. (A) Primary human neutrophils were stimulated with PVL (100 nM), PMA (100 nM), or nigericin (30 µM) for 4 h to induce NETs. MRSA was incubated with these NETs for 1 h and colony-forming units was quantified after overnight incubation on TSA plates. Bacterial viability is expressed as a percentage of colony-forming units normalized to MRSA incubated in the absence of NETs. (B) The DNA content of PVL-, PMA-, and nigericin-induced NETs at 4 h was quantified by spectrophotometry. (A) Mean ± SD of 5 independent experiments. *P < 0.05, *** P < 0.001, 1-way analysis of variance. (B) Mean ± SD of 4 independent experiments. ns = not significant.

Techniques Used: Incubation, Spectrophotometry

Fig. 4. Neutrophils from patients with recurrent PVL-SA infections make more NETs in response to PVL and express more CD45 than neutrophils from healthy donors. (A) Purified primary neutrophils from patients experiencing recurrent PVL-SA infections (n = 19) and healthy control individuals (n = 19) were either left untreated or stimulated with PMA (50 nM) or PVL (0.1 nM, 1 nM, or 10 nM) for 4 h, and cell death was quantified by adding the cell-impermeable DNA dye SYTOX Green and measuring fluorescence. The boxplot indicates SYTOX fluorescence relative to naïve neutrophils at 4 h. (B) CD45, C5L2, CD88, CD63, and CD66b were immunolabelled on neutrophils from patients and healthy control individuals. The fluorescence was measured and indicated as log-transformed mean fluorescence intensity (MFI). (C) CD45 or (D) C5L2 fluorescence of patient neutrophils relative to control neutrophils was plotted against SYTOX fluorescence of patient neutrophils relative to control neutrophils after incubation with 0.1 nM PVL for 4 h. (A) Unpaired Wilcoxon signed rank test with Bonferroni post hoc test, *P < 0.05. (B) Paired t test, ****P < 0.0001. (C, D) Spearman’s correlation test in which the coefficient of correlation (ρ) and probability (P) are indicated. A best-fit line indicates the trend.

Figure Legend Snippet: Fig. 4. Neutrophils from patients with recurrent PVL-SA infections make more NETs in response to PVL and express more CD45 than neutrophils from healthy donors. (A) Purified primary neutrophils from patients experiencing recurrent PVL-SA infections (n = 19) and healthy control individuals (n = 19) were either left untreated or stimulated with PMA (50 nM) or PVL (0.1 nM, 1 nM, or 10 nM) for 4 h, and cell death was quantified by adding the cell-impermeable DNA dye SYTOX Green and measuring fluorescence. The boxplot indicates SYTOX fluorescence relative to naïve neutrophils at 4 h. (B) CD45, C5L2, CD88, CD63, and CD66b were immunolabelled on neutrophils from patients and healthy control individuals. The fluorescence was measured and indicated as log-transformed mean fluorescence intensity (MFI). (C) CD45 or (D) C5L2 fluorescence of patient neutrophils relative to control neutrophils was plotted against SYTOX fluorescence of patient neutrophils relative to control neutrophils after incubation with 0.1 nM PVL for 4 h. (A) Unpaired Wilcoxon signed rank test with Bonferroni post hoc test, *P < 0.05. (B) Paired t test, ****P < 0.0001. (C, D) Spearman’s correlation test in which the coefficient of correlation (ρ) and probability (P) are indicated. A best-fit line indicates the trend.

Techniques Used: Purification, Control, Fluorescence, Transformation Assay, Incubation

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Journal: Journal of leukocyte biology

doi: 10.1093/jleuko/qiad137

Figure Lengend Snippet: Fig. 1. PVL induces ROS-independent NET formation. (A, B) ROS formation was quantified in control (A: n = 14, B: n = 3) or CGD human (n = 3) primary neutrophils stimulated with PMA (50 nM) or PVL (0.1 nM, 1 nM or 10 nM). (C) Control or CGD neutrophils were stimulated with PMA (50 nM) or PVL (10 nM) for 3 h, and cell death was quantified using the cell-impermeable DNA dye SYTOX Green. Indicated is SYTOX Green fluorescence relative to t = 0 min. (D) Representative confocal microscopy images of control and CGD patient neutrophils either naïve or stimulated with PMA (50 nM) or PVL (1 nM or 10 nM) and stained for DNA (blue), NE (red), and chromatin (green). The scale bar represents 10 µm. (E–G) Healthy human neutrophils were treated with PKC inhibitor Gö6983 (1 μM), BAPTA-AM (10 μM), DPI (1 μM), pyrocatechol (30 μM), ABAH (500 μM), NEi (20 μM), and AEBSF (100 μM) for 30 min, before stimulating with (E) PVL 1 nM, (F) PVL 10 nM, or (G) PMA 50 nM for 4 h. We quantified cell death with SYTOX Green and the fluorescence signal relative to naïve is indicated. (H) Representative confocal microscopy of naïve neutrophils or after stimulation with PMA or PVL (1 nM or 10 nM) in the presence or absence of indicated inhibitors, and stained for DNA (blue), NE (red), and chromatin (green). The scale bar represents 10 µm. (C) Two-way analysis of variance with Tukey’s post hoc test. *P < 0.05, ***P < 0.001. (E–G) Mean ± SD of 4 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, 1-way analysis of variance with Dunnett’s multiple comparison test. ns = not significant.

Article Snippet: We used the following inhibitors: Gö6983 (protein kinase C [PKC] inhibitor; Tocris) BAPTA-AM (Thermo Fisher Scientific), pyrocatechol (Sigma-Aldrich), ABAH (Cayman chemical), neutrophil elastase (NE) inhibitor (NEi) (MedChemExpress), DPI (Calbiochem), AEBSF (Sigma-Aldrich), allopurinol (Sigma-Aldrich), Apamin (Sigma-Aldrich), DNP (Sigma-Aldrich) and FCCP (Abcam).

Techniques: Control, Fluorescence, Confocal Microscopy, Staining, Comparison

Journal: Journal of leukocyte biology

doi: 10.1093/jleuko/qiad137

Figure Lengend Snippet: Fig. 2. NET proteome assembly is different in PVL-induced NETs. (A) Principal component analysis of the proteomes of naïve neutrophils, and PVL-induced (10 nM), PMA-induced (50 nM), and nigericin-induced (15 µM) NETs. Analysis was performed on scaled log2-abundance of all proteins detected in at least 2 of 3 replicates. (B) Euler diagram showing the number and distribution of significant differentially abundant peptides (logFC > 1, adjusted P < 0.01) on NETs compared with naïve neutrophils. Areas are proportional to DAP set size. (C) Clustered heatmap showing fold change (log2) values on each NET sample compared with naïve neutrophils of significant DAPs from panel B. Clustering was performed by k-means algorithm with k = 4 clusters. (D, E) Top 25 most abundant DAPs that are significantly differentially abundant on PVL-induced NETs compared with PMA-induced (D) and nigericin-induced NETs (E). Point size and fill color represent average abundance across samples and adjusted P value, respectively. Proteomes were made from n = 3 samples per condition from independent donors. DAP significance for each comparison was determined by a threshold of |[log2 fold change]| > 1 and adjusted P value < 0.01.

Techniques: Comparison

Journal: Journal of leukocyte biology

doi: 10.1093/jleuko/qiad137

Figure Lengend Snippet: Fig. 3. PVL-induced NETs do not kill MRSA. (A) Primary human neutrophils were stimulated with PVL (100 nM), PMA (100 nM), or nigericin (30 µM) for 4 h to induce NETs. MRSA was incubated with these NETs for 1 h and colony-forming units was quantified after overnight incubation on TSA plates. Bacterial viability is expressed as a percentage of colony-forming units normalized to MRSA incubated in the absence of NETs. (B) The DNA content of PVL-, PMA-, and nigericin-induced NETs at 4 h was quantified by spectrophotometry. (A) Mean ± SD of 5 independent experiments. *P < 0.05, *** P < 0.001, 1-way analysis of variance. (B) Mean ± SD of 4 independent experiments. ns = not significant.

Techniques: Incubation, Spectrophotometry

Journal: Journal of leukocyte biology

doi: 10.1093/jleuko/qiad137

Figure Lengend Snippet: Fig. 4. Neutrophils from patients with recurrent PVL-SA infections make more NETs in response to PVL and express more CD45 than neutrophils from healthy donors. (A) Purified primary neutrophils from patients experiencing recurrent PVL-SA infections (n = 19) and healthy control individuals (n = 19) were either left untreated or stimulated with PMA (50 nM) or PVL (0.1 nM, 1 nM, or 10 nM) for 4 h, and cell death was quantified by adding the cell-impermeable DNA dye SYTOX Green and measuring fluorescence. The boxplot indicates SYTOX fluorescence relative to naïve neutrophils at 4 h. (B) CD45, C5L2, CD88, CD63, and CD66b were immunolabelled on neutrophils from patients and healthy control individuals. The fluorescence was measured and indicated as log-transformed mean fluorescence intensity (MFI). (C) CD45 or (D) C5L2 fluorescence of patient neutrophils relative to control neutrophils was plotted against SYTOX fluorescence of patient neutrophils relative to control neutrophils after incubation with 0.1 nM PVL for 4 h. (A) Unpaired Wilcoxon signed rank test with Bonferroni post hoc test, *P < 0.05. (B) Paired t test, ****P < 0.0001. (C, D) Spearman’s correlation test in which the coefficient of correlation (ρ) and probability (P) are indicated. A best-fit line indicates the trend.

Techniques: Purification, Control, Fluorescence, Transformation Assay, Incubation

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