Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Bioinformatics analysis prioritized PTGS2 and MMP9 as candidate inflammatory genes associated with the IL-17 signaling pathway in ischemic stroke. (A) Venn diagram showing the overlap between differentially expressed genes (DEGs) identified from GEO datasets and genes retrieved from the CellAge database. Five overlapping genes were identified: PTGS2, MMP9, SERPINB2, CTNNAL1, and HTRA1. CS, genes from CellAge database; DEG, significantly differentially expressed genes in ischemic stroke. (B) Gene Ontology (GO) enrichment analysis of the overlapping genes, including biological process, cellular component, and molecular function categories. (C) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis showing that the overlapping genes were enriched in inflammation-related pathways, including the IL-17 signaling pathway and TNF signaling pathway. (D) GSEA comparing ischemic stroke (IS) and control samples, demonstrating enrichment of immune- and inflammation-related pathways in IS. (E) Predicted transcription factor–target gene regulatory network for PTGS2 and MMP9, showing candidate shared upstream transcription factors. Yellow nodes represent TFs, red nodes represent target genes.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Control

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Serum IL-17A, PTGS2, and MMP9 levels in the clinical cohort and their correlations with each other and with stroke severity. (A–C) Serum IL-17A, PTGS2, and MMP9 levels were significantly higher in patients with ischemic stroke than in healthy controls. IS, ischemic stroke (n = 104); Normal, control group (n = 58). (D) Correlations among serum IL-17A, PTGS2, and MMP9 levels in the stroke group. (E) Positive correlations between serum IL-17A, PTGS2, and MMP9 levels and admission NIHSS scores in patients with ischemic stroke. Correlations were analyzed using Spearman’s rank correlation test. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Control

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: MCAO-induced activation of IL-17A/PTGS2/MMP9-related inflammatory markers and changes after anti-IL-17A antibody treatment in rat brain tissue. (A–C) Relative mRNA levels of PTGS2, MMP9, and IL-17A in the sham, MCAO, and anti-IL-17A Ab groups. (D–F) Protein concentrations of PTGS2, MMP9, and IL-17A. (G, H) Concentrations of PGE2 and IL-6. (I) Neurological deficit scores assessed using the Longa scoring system. In panel I, the sham group median was 0; therefore, a minimal bar height was displayed for visualization only. (J) Representative TTC-stained brain sections from the MCAO and anti-IL-17A Ab groups. White areas indicate infarct regions, whereas red areas indicate viable brain tissue. (K) Quantitative analysis of infarct volume percentage based on TTC staining. Sham, sham-operated group; Model, MCAO group; anti-IL-17A Ab, IL-17A neutralizing antibody-treated MCAO group. Data in panels A-H are presented as mean ± SEM (n = 6 per group). Neurological deficit scores in panel I are presented as median (interquartile range) (n = 6 per group). TTC analysis in panels (J, K) was performed in an independent cohort of rats, with final sample sizes of n = 4 for the MCAO group and n = 5 for the anti-IL-17A Ab group; one rat in the MCAO group died before tissue collection. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Activation Assay, Staining

Journal: Frontiers in Immunology

Article Title: IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence

doi: 10.3389/fimmu.2026.1812571

Figure Lengend Snippet: Spearman correlation analyses among IL-17A, PTGS2, MMP9, PGE2, and IL-6 in rat brain tissue. Correlation analyses were performed using pooled data from all animals (n = 18). (A) Correlation between IL-17A and PTGS2 mRNA expression. (B) Correlation between IL-17A and MMP9 mRNA expression. (C) Correlation between IL-17A and PTGS2 protein expression. (D) Correlation between IL-17A and MMP9 protein expression. (E) Correlation between IL-17A and PGE2 levels. (F) Correlation between IL-17A and IL-6 levels. Sham, sham-operated group; Model, MCAO group; anti-IL-17A Ab, IL-17A neutralizing antibody-treated MCAO group. Given the limited sample size, these correlations should be interpreted with caution.

Article Snippet: Rats in the IL-17A neutralizing antibody-treated group were treated with Anti-Mouse/Rat IL-17A Antibody (17F3; MedChemExpress, Cat. No. HY-P990222), a mouse IgG1κ monoclonal neutralizing antibody against mouse/rat IL-17A, via intravenous injection at 100 μg/rat immediately after reperfusion and again at 12 h post-reperfusion.

Techniques: Expressing

Journal: Immunology letters

Article Title: A lack of confirmation with alternative assays questions the validity of IL-17A expression in human neutrophils using immunohistochemistry.

doi: 10.1016/j.imlet.2014.10.025

Figure Lengend Snippet: Fig. 1. Detection of IL-17A in human neutrophils by IHC. (A) Cyanine3 labelled IL-17A+ cells infiltrate Wolbachia-containing nodules but not Wolbachia-depleted nodules. (B) Counterstaining

Article Snippet: Immunoprecipitation was carried out using 100 g mouse anti-human IL-17A antibody (41802, R&D Systems) and 60 g goat anti-human IL-17A antibody (AF-317-NA, R&D Systems) coupled to 1 mL HiTrap NHS-activated HP columns and AKTAprime Plus low-pressure affinity chromatography system (both from GE Healthcare) using the manufacturer’s protocol.

Techniques:

Journal: Immunology letters

Article Title: A lack of confirmation with alternative assays questions the validity of IL-17A expression in human neutrophils using immunohistochemistry.

doi: 10.1016/j.imlet.2014.10.025

Figure Lengend Snippet: Fig. 2. Determination of IL-17A expression by human neutrophils. (A) Western blotting of neutrophil (PMN) cell lysate using goat anti-IL-17A antibody and mouse anti- IL-17A antibody.

Article Snippet: Immunoprecipitation was carried out using 100 g mouse anti-human IL-17A antibody (41802, R&D Systems) and 60 g goat anti-human IL-17A antibody (AF-317-NA, R&D Systems) coupled to 1 mL HiTrap NHS-activated HP columns and AKTAprime Plus low-pressure affinity chromatography system (both from GE Healthcare) using the manufacturer’s protocol.

Techniques: Expressing, Western Blot

Journal: Biomedicines

Article Title: Acetylated Diacylglycerol 1-palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol in Autoimmune Arthritis and Interstitial Lung Disease in SKG Mice

doi: 10.3390/biomedicines9091095

Figure Lengend Snippet: Histologic examination of the lung tissue from SKG mice at 20 weeks after a curdlan injection with/without PLAG treatment. ( A ) Hematoxylin and eosin (upper panels) and Masson’s trichrome (lower panels) staining of the lung tissues. Severe lung inflammations were observed in the curdlan-induced SKG mice and these features were attenuated in the PLAG-treated curdlan-induced SKG mice. ( B ) Opal multiplexed immunofluorescent images and semi-quantitation of the total, GM-CSF + and IL-17A + neutrophil accumulation in the lung tissues. The GM-CSF + neutrophil accumulation was significantly decreased in the PLAG-treated curdlan-induced SKG mice compared with those without PLAG treatment whereas the IL-17A + neutrophil accumulation was not attenuated. The values represent the mean of three independent experiments ± SEM. * p < 0.05. PLAG: acetylated diacylglycerol 1-palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol.

Article Snippet: The slides were again placed in a citrate buffer (pH 6.0), heated in a microwave and incubated with primary rabbit antibodies for IL-17A (Novus Biologicals, Centennial, CO, USA, NBP1-76337, 1:500) for 1 h in a humidified chamber at RT followed by a detection using polymer HRP Ms + Rb.

Techniques: Injection, Staining, Quantitation Assay

Journal: Bioactive Materials

Article Title: Engineering a halloysite nanotube-enhanced hydrogel 3D skin model for modulated inflammation and accelerated wound healing

doi: 10.1016/j.bioactmat.2024.11.013

Figure Lengend Snippet: Viability and functionality assessment of HFFs in HNT-modified hydrogel (a) Representative images and percentage of HFFs positive for vimentin by IF staining on days 0, 3, and 7 in natural hydrogel and 1 μg/mL HNT-based hydrogel. Data are represented as mean ± SD. ∗ P < 0.05 (two-way ANOVA analysis). Scale bar = 20 μm. (b) Relative expression levels of talin2, plasminogen, fibronectin, and paxillin assessed by RT-PCR tests in cultured HFFs on day 3. Each dot represents one independent experiment. Data are represented as mean ± SD. ns, not significant, ∗ P < 0.05; ∗∗ P < 0.01 (unpaired Student's t-test). (c) Representative images and percentage of HFFs positive for vimentin by IF staining in natural hydrogel and 1 μg/mL HNT-based hydrogel. The cells were stimulated with cytokines (TNF-α, IL-17A, and IL-22) in different concentrations (0, 25, 50, 100 ng/mL). Scale bar = 100 μm. (d) Representative 3D images from the top view of HFFs positive for vimentin in I collagen-based hydrogel, natural hydrogel, and 1 μg/mL HNT-based hydrogel on days 1, 3 and 7. The cells were stimulated without or with cytokines (TNF-α, IL-17A, and IL-22, 50 ng/mL for each cytokine). Scale bar = 100 μm. (e) Relative expression levels of vimentin in HFFs in I collagen-based hydrogel, natural hydrogel, and 1 μg/mL HNT-based hydrogel on days 1, 3, and 7 without cytokine stimulation. Data are represented as mean ± SD. ∗ P < 0.05 (two-way ANOVA analysis). (f) Relative expression levels of vimentin in HFFs in I collagen-based hydrogel, natural hydrogel, and 1 μg/mL HNT-based hydrogel on days 1, 3, and 7 with cytokine (TNF-α, IL-17A, and IL-22, 50 ng/mL for each) stimulation. Data are represented as mean ± SD. ∗∗ P < 0.01 (two-way ANOVA analysis).

Article Snippet: Subsequently, the samples were incubated overnight at 4 °C with primary antibodies, including rabbit anti-Ki-67 (catalog #34330, CST, USA), keratin (K) 5 (catalog # 71536, CST, USA), vimentin (catalog # 10366-1-AP, Proteintech, China), fibronectin (catalog # 15613-1-AP, Proteintech, China), K17 (catalog # 17516-1-AP, Proteintech, China), mouse anti-K10 (catalog # ab9025, Abcam, UK), CD34 (catalog # 31120-1-AP, Proteintech, China), or IL-17A (catalog # 66148-1-Ig, Proteintech, China).

Techniques: Modification, Staining, Expressing, Reverse Transcription Polymerase Chain Reaction, Cell Culture

Journal: Bioactive Materials

Article Title: Engineering a halloysite nanotube-enhanced hydrogel 3D skin model for modulated inflammation and accelerated wound healing

doi: 10.1016/j.bioactmat.2024.11.013

Figure Lengend Snippet: Inflammatory bioactivity of modified hydrogel and its potential for cell proliferation, migration, and adhesion. (a) Schematic of RNA-seq of the HFFs in hydrogel group. Four groups were set as group A (without HNT), group B (with HNT of 1 μg/mL), group C (without HNT, stimulated with TNF-α, IL-17A, and IL-22, 50 ng/mL) and group D (with HNT of 1 μg/mL, stimulated with with TNF-α, IL-17A, and IL-22, 50 ng/mL). (b) Heatmap of relative expression levels of genes associated with inflammation, proliferation and migration in group B (with HNT) compared to group A (without HNT). (c) KEGG pathway analysis of enriched genes showing the relevant functional terms in group D compared to group B. (d) Specific inflammatory clusters of genes related to KEGG analysis showing the relevant functional terms in group D compared to group B. (e) KEGG pathway analysis of enriched genes showing the relevant functional terms in group A compared to group C as well as group D compared to group B. (f) Venn diagram of differentially expressed genes overlapped in the four groups. (g) Representative 3D images of K17 expression in upper-layer from the top and side-view of the modified 3D skin model. (h) Relative expression levels of K17 in 0 μg/mL and 1 μg/mL HNT-based hydrogel with cytokine (TNF-α, IL-17A, and IL-22, 50 ng/mL) stimulation. Each dot represents one independent experiment. Data are represented as mean ± SD. ∗ P < 0.05 (unpaired student's t-test).

Article Snippet: Subsequently, the samples were incubated overnight at 4 °C with primary antibodies, including rabbit anti-Ki-67 (catalog #34330, CST, USA), keratin (K) 5 (catalog # 71536, CST, USA), vimentin (catalog # 10366-1-AP, Proteintech, China), fibronectin (catalog # 15613-1-AP, Proteintech, China), K17 (catalog # 17516-1-AP, Proteintech, China), mouse anti-K10 (catalog # ab9025, Abcam, UK), CD34 (catalog # 31120-1-AP, Proteintech, China), or IL-17A (catalog # 66148-1-Ig, Proteintech, China).

Techniques: Modification, Migration, RNA Sequencing, Expressing, Functional Assay

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: Primers sequences used for qPCR analysis.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques:

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: IL-17A, IL-17F, IL-17 receptor and IL-17 target genes are transcriptionally upregulated following in vivo I/R injury. RNA and protein was extracted from the left ventricles of rats undergoing sham operation or 25 min ischaemia and 2 h reperfusion (I/R). (A) IL-17RA, IL-17A and IL-17F expression was measured by qPCR. (B) IL-17A and IL-17RA protein levels were assessed by western blot, GAPDH was used as a loading control. (C) Expression of the IL-17 target genes IL-6, IL-1, iNOS and MMP-9 was measured by qPCR.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: In Vivo, Expressing, Western Blot, Control

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: IL-17 induces Cxcl1, IL-6 and Socs3 expression in cardiac myocytes. Neonatal rat ventricular myocytes were treated with 10 ng/ml IL-17 for the indicated times and the levels of (A) Cxcl1, (B) IL-6, (C) MCP-1 and (D) Socs3 were measured by qPCR. Experiments were repeated in duplicate, statistical analysis was carried out using a one-way ANOVA followed by Dunnett's post test, *p < 0.05, **p < 0.01, ***p < 0.001. (E) I/R injury and IL-17 have additive effects on Cxcl1 expression. NRVMs were subjected to 4 h ischaemia and 6 h reperfusion with or without 10 ng/ml IL-17 which was added at the time of reperfusion. The expression of Cxcl1 was analysed by qPCR. Statistical analysis was carried out using student's t -test. **p < 0.01, **p < 0.001.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: Expressing

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: IL-17 mediated upregulation of Cxcl1 and IL-6 in cardiac myocytes is MAPK dependent. (A) NRVMs were treated with 10 ng/ml IL-17 for the indicated times and cell lysates were analysed by Western blot using the indicated antibodies. (B) NRVMs were pre-treated for 30 min with the indicated inhibitors followed by IL-17 stimulation for 6 h. The expression of Cxcl1 and IL-6 was measured by qPCR. Statistical analysis was carried out using a student's t -test. *p < 0.05, **p < 0.01, **p < 0.001.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: Western Blot, Expressing

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: IL-17 receptor and IL-17F are transcriptionally upregulated in cardiac myocytes. (A) NRVM were subjected to 4 h in vitro ischaemia and up to 24 h reperfusion in normal media after which the levels of IL-17 receptor and IL-17F were assessed by qPCR. (B) H9c2 cells were subjected to in vitro I/R for the indicated times and the levels of IL-17F and Cxcl1 were measured by qPCR. (C) NRVMs were treated with 200 μM H 2 O 2 for 6 h and the expression of the indicated genes was measured by qPCR. (D) NRMVs were transduced with STAT3C adenovirus at MOI = 100. After 48 h, increased expression of STAT3 was confirmed by Western blot and IL-17F expression was measured by qPCR. *p < 0.05, **p < 0.01, ***p < 0.001, student's t -test, n = 3 per group, repeated in duplicate.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: In Vitro, Expressing, Transduction, Western Blot

Journal: International Journal of Cardiology

Article Title: Enhanced IL-17 signalling following myocardial ischaemia/reperfusion injury

doi: 10.1016/j.ijcard.2011.08.849

Figure Lengend Snippet: Blocking IL-17 signalling with a specific anti-IL-17 neutralizing antibody reduced creatine phosphokinase and apoptotic cell death in the myocardium following in vivo I/R injury. Plasma concentration of CPK (A) and apoptosis assessed by the TUNEL assay (B) in sham-operated (control) or rats exposed to in vivo I/R injury (I/R) or I/R plus treatment with IL-17 neutralizing antibody (IL-17 Bo Ab). Immunofluorescence data (left panel) (Data are mean of ± 6 rats **P < 0.001). Anti-IL-17 neutralizing antibody also reduced the increase in cleaved/active caspase-3 expression following in vivo I/R injury (C). Western blot analysis was performed on tissue lysates prepared as in Fig. 3 A above and immunoblotted with a specific antibody against the cleaved and active form of caspase-3 and GAPDH.

Article Snippet: In a different set of experiments rats were treated with 200 μg of anti-IL-17A polyclonal antibody intraperitoneally (R & D Systems, AF-421-NA) or PBS 2 h before undergoing in vivo ischemia/reperfusion injury.

Techniques: Blocking Assay, In Vivo, Clinical Proteomics, Concentration Assay, TUNEL Assay, Control, Immunofluorescence, Expressing, Western Blot