Journal: Nature Communications

Article Title: A montmorillonite-based oral fermentation system enables long-lasting in-situ biosynthesis to restore intestinal homeostasis

doi: 10.1038/s41467-026-69071-2

Figure Lengend Snippet: After 24 hours of LPS (1 µg/ml) stimulation, J774A.1 cells were incubated with culture medium, Bac, MMT@Bac, MMT@Bac@T, MMT@Bac@L, or MMT@Bac@TL for 24 hours. Cells without any treatment were set as a control. a , b Flow cytometric analyses of ( a ) M2 and ( b ) M1 macrophages. c , d Percentages of M2 ( c ) and M1 ( d ) macrophages. e Ratio of M2 to M1 macrophages ( n = 5 or 6 independent samples). f – h Concentrations of IL-1β ( f ), TGF-β ( g ), and VEGF ( h ) in the supernatant ( n = 4, 5 or 6 independent samples). Mice pretreated with an antibiotic cocktail were administered with PBS, Bac, MMT@Bac, MMT@Bac@T, MMT@Bac@L, or MMT@Bac@TL one dose per day for 7 days. i , j Percentages of M2 macrophages ( i ) and mature DCs ( j ) in the MLNs ( n = 6 independent samples). k Percentage of IgA + B cells in the PPs ( n = 4-6 independent samples). Data are represented as means ± SD. p- values were determined using one-way ANOVA. p- values < 0.05 are shown. Source data are provided as a Source Data file.

Article Snippet: IL-4 (AF02165-A), IL-6 (AF02163-A), and IL-10 (AF02176-A) enzyme-linked immunosorbent assay (ELISA) kits were purchased from Hunan Aifang Biotechnology Co., Ltd. VEGF (EK283), IL-1β (EK201B), and TGF-β1 (EK981) ELISA kits were obtained from Multi Sciences (Lianke) Biotech Co., Ltd.

Techniques: Incubation, Control

Journal: Frontiers in Immunology

Article Title: Putative α7-selective ligands interact with α9-containing nicotinic acetylcholine receptors and modulate immune functions of human mononuclear phagocytes

doi: 10.3389/fimmu.2026.1773637

Figure Lengend Snippet: Chemical structures of the molecules investigated to modulate the ATP-induced release of the pro-inflammatory cytokine interleukin (IL)-1β by mononuclear phagocytes.

Article Snippet: IL-1α/β-equivalent bioactive concentrations (pg/ml) were determined by interpolation from a 4-parameter logistic standard curve generated with a serial dilution of recombinant human IL-1β (InvivoGen, Cat# rcyc-hil1b) that was dissolved in FBS-free RPMI 1640 medium and run in parallel with the samples.

Techniques:

Journal: Frontiers in Immunology

Article Title: Putative α7-selective ligands interact with α9-containing nicotinic acetylcholine receptors and modulate immune functions of human mononuclear phagocytes

doi: 10.3389/fimmu.2026.1773637

Figure Lengend Snippet: The putative α7-selective nicotinic acetylcholine receptor (nAChR) agonists S24795 (S24) and PNU-282987 (PNU) inhibit the BzATP-mediated interleukin (IL)-1β release. Monocytic THP-1 cells and THP-1 cell-derived M1-like macrophages were primed for 5 h with lipopolysaccharide (LPS; 1 µg/ml). The P2X7 receptor agonist BzATP was added for another 40 min to trigger IL-1β release, which was quantified by ELISA (A,C) and by measuring IL-1α/β-equivalent bioactive concentrations using HEK-Blue™ IL-1R cells in a QUANTI-Blue™ assay (B, D) . The BzATP- (100 µM) induced release of IL-1β was investigated in the presence and absence of the nAChR agonists S24 (50 µM) and PNU (10 µM), acetylcholine (ACh, 10 µM) or phosphocholine (PC, 200 µM). The amount of IL-1β released in response to BzATP was calculated by subtracting the IL-1β concentrations of cells treated with LPS alone. In each experiment, the IL-1β concentrations obtained after stimulation with BzATP were set to 100% and all other values were calculated accordingly. Data are presented as individual data points, bars represent median, whiskers percentiles 25 and 75. *p ≤ 0.05, different from LPS-primed cells stimulated with BzATP alone. Friedman test followed by the Wilcoxon signed-rank test.

Article Snippet: IL-1α/β-equivalent bioactive concentrations (pg/ml) were determined by interpolation from a 4-parameter logistic standard curve generated with a serial dilution of recombinant human IL-1β (InvivoGen, Cat# rcyc-hil1b) that was dissolved in FBS-free RPMI 1640 medium and run in parallel with the samples.

Techniques: Derivative Assay, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: Putative α7-selective ligands interact with α9-containing nicotinic acetylcholine receptors and modulate immune functions of human mononuclear phagocytes

doi: 10.3389/fimmu.2026.1773637

Figure Lengend Snippet: The effect of α7 nicotinic acetylcholine receptor (nAChR) agonists S24795 (S24) and PNU-282987 (PNU) on the BzATP-mediated release of interleukin (IL)-1β is sensitive to methyllycaconitine (MLA). Monocytic THP-1 cells (A) and THP-1 cell-derived M1-like macrophages (B) were primed for 5 h with LPS (LPS; 1 µg/ml). The P2X7 receptor agonist BzATP was added for another 40 min to trigger IL-1β release, which was measured by ELISA. The BzATP- (100 µM) induced release of IL-1β was investigated in the presence and absence of the nAChR agonists S24 (50 µM) and PNU (10 µM), or the ligands acetylcholine (ACh, 10 µM) and phosphocholine (PC, 200 µM). In addition, MLA was co-applied. The amount of IL-1β released in response to BzATP was calculated by subtracting the IL-1β concentrations measured in supernatants of cells treated with LPS alone. In each experiment, the IL-1β concentrations obtained after stimulation with BzATP were set to 100% and all other values were calculated accordingly. Data are presented as individual data points, bars represent median, whiskers percentiles 25 and 75. *p ≤ 0.05, different from LPS-primed cells stimulated with BzATP alone; #p ≤ 0.05, different from LPS-primed cells stimulated with BzATP plus an agonist. Friedman test followed by the Wilcoxon signed-rank test.

Article Snippet: IL-1α/β-equivalent bioactive concentrations (pg/ml) were determined by interpolation from a 4-parameter logistic standard curve generated with a serial dilution of recombinant human IL-1β (InvivoGen, Cat# rcyc-hil1b) that was dissolved in FBS-free RPMI 1640 medium and run in parallel with the samples.

Techniques: Derivative Assay, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in Immunology

Article Title: Putative α7-selective ligands interact with α9-containing nicotinic acetylcholine receptors and modulate immune functions of human mononuclear phagocytes

doi: 10.3389/fimmu.2026.1773637

Figure Lengend Snippet: The effect of the putative α7-selective nicotinic acetylcholine receptor (nAChR) agonists S24795 (S24) and PNU-282987 (PNU) on the BzATP-mediated cytokine release is sensitive to the α-conopeptides [V11L,V16D]ArIB and RgIA4. Monocytic THP-1 cells and THP-1 cell-derived M1-like macrophages were primed for 5 h with LPS (LPS; 1 µg/ml). The P2X7 receptor agonist BzATP was added for another 40 min to trigger the release of IL-1β (A, C) and IL-18 (B, D) , which was measured by ELISA. The BzATP- (100 µM) induced release of IL-1β and IL-18 was investigated in the presence and absence of the α7 nAChR agonists S24 (50 µM) and PNU (10 µM). To test for the involvement of nAChR subunits the conopeptides Rg1A4 (RgIA; 200 nM) or [V11L,V16D]ArIB (500 nM) were co-applied. The amount of IL-1β and IL-18 released in response to BzATP was calculated by subtracting the IL-1β concentrations measured in supernatants of cells treated with LPS alone. In each experiment, the IL-1β concentrations obtained after stimulation with BzATP were set to 100% and all other values were calculated accordingly. Data are presented as individual data points, bars represent median, whiskers percentiles 25 and 75. *p ≤ 0.05, different from LPS-primed cells stimulated with BzATP alone; #p ≤ 0.05, different from LPS-primed cells stimulated with BzATP plus an agonist. Friedman test followed by the Wilcoxon signed-rank test.

Article Snippet: IL-1α/β-equivalent bioactive concentrations (pg/ml) were determined by interpolation from a 4-parameter logistic standard curve generated with a serial dilution of recombinant human IL-1β (InvivoGen, Cat# rcyc-hil1b) that was dissolved in FBS-free RPMI 1640 medium and run in parallel with the samples.

Techniques: Derivative Assay, Enzyme-linked Immunosorbent Assay

Journal: Frontiers in endocrinology

Article Title: Excessive Iodine Promotes Pyroptosis of Thyroid Follicular Epithelial Cells in Hashimoto's Thyroiditis Through the ROS-NF-κB-NLRP3 Pathway.

doi: 10.3389/fendo.2019.00778

Figure Lengend Snippet: FIGURE 1 | Aberrant pyroptosis occurs in the thyroid tissues of HT patients and is induced by excessive iodine in vitro. (A,B) Gasdermin D (GSDMD) protein levels in the thyroid tissue of HT patients (n = 20) and controls (n = 10) were analyzed by immunoblots. “Control” indicates tissues from patients with nodular goiter of the thyroid. Representative immunoblotting results and quantification of GSDMD are shown. (C,D) Representative results of GSDMD immunohistochemical staining in HT tissues (n = 20) and control tissues (n = 10) are shown. Brown regions represent positive expression (original magnification, ×200; scale bars, 100 µm). (E–G) Nthy-ori3-1 cells were harvested after treatment with a gradient of concentrations of sodium iodide (NaI) for 24 h. The images presented are immunoblots probed for GSDMD (Hsp60 served as the loading control). All statistical results shown are representative of three replicates. (H) The cell viability of Nthy-ori 3-1 cells was assessed by CCK-8 assays after NaI treatment for 24 h. All statistical results shown are representative of three replicates. Significant differences and P-values were calculated by unpaired t-tests or one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Thyroid sections were blocked with 2% bovine serum albumin in PBS for 30min and then incubated with mouse anti-human GSDMD or mouse antihuman IL-1β antibodies (Santa Cruz, NJ, USA) at 4◦C overnight.

Techniques: In Vitro, Western Blot, Control, Immunohistochemical staining, Staining, Expressing, CCK-8 Assay

Journal: Frontiers in endocrinology

Article Title: Excessive Iodine Promotes Pyroptosis of Thyroid Follicular Epithelial Cells in Hashimoto's Thyroiditis Through the ROS-NF-κB-NLRP3 Pathway.

doi: 10.3389/fendo.2019.00778

Figure Lengend Snippet: FIGURE 3 | The NLRP3 inflammasome participates in excessive iodine-induced pyroptosis in TFCs. (A,B) The NLRP3 expression levels were measured by immunoblots when Nthy-ori 3-1 cells were treated with NaI with or without NAC (10 mM) or IKK-16 (2 µM) for 24 h. (C,D) Verification of the silencing efficiency of NLRP3 by siRNA in Nthy-ori3-1 cells is shown by immunoblots; NC indicates the negative control. (E,F) The protein levels of GSDMD were detected by immunoblots after transfection of siNLRP3 in NaI-treated Nthy-ori 3-1 cells. All statistical results shown are representative of three replicates. Significant differences and P-values were calculated by one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: Thyroid sections were blocked with 2% bovine serum albumin in PBS for 30min and then incubated with mouse anti-human GSDMD or mouse antihuman IL-1β antibodies (Santa Cruz, NJ, USA) at 4◦C overnight.

Techniques: Expressing, Western Blot, Negative Control, Transfection

Journal: Frontiers in endocrinology

Article Title: Excessive Iodine Promotes Pyroptosis of Thyroid Follicular Epithelial Cells in Hashimoto's Thyroiditis Through the ROS-NF-κB-NLRP3 Pathway.

doi: 10.3389/fendo.2019.00778

Figure Lengend Snippet: FIGURE 5 | Proposed model of TFC pyroptosis in excessive iodine-promoted HT. Excessive iodine enters TFCs and induces the production of ROS, which activates NF-κB signaling and increases GSDMD-FL. In addition, the NLRP3 inflammasome is activated by NF-κB signaling, leading to GSDMD-FL cleavage into GSDMD-N, which triggers pore formation in the membrane and the release of mature IL-1β from cells, causing a sterile inflammatory response and further contributing to pyroptotic cell death and the subsequent promotion of HT.

Article Snippet: Thyroid sections were blocked with 2% bovine serum albumin in PBS for 30min and then incubated with mouse anti-human GSDMD or mouse antihuman IL-1β antibodies (Santa Cruz, NJ, USA) at 4◦C overnight.

Techniques: Membrane, Sterility