Journal: BMC Gastroenterology

Article Title: Inhibition of TLR4 enhances oxaliplatin chemotherapy sensitivity in esophageal squamous cell carcinoma by suppressing inflammation and glycolysis

doi: 10.1186/s12876-026-04663-2

Figure Lengend Snippet: OXA activated TLR4 signaling in ESCC cells. The cells were treated by OXA (25 µM) for 24 h. A , B . The mRNA expressions of TLR4 and MYD88 in ESCC cell lines and normal esophageal cells were detected by qRT-PCR. C . ICC showed the immunocytochemical activity of NF-κB p65, p-NF-κB p65, COX-2, and MYD88. Scale bar: 50 μm. D . qRT-PCR analysis of mRNA levels of IL-1β, IL-6, COX-2, CXCL5, and CXCL8. *p < 0.05, **p < 0.01, ***p < 0.001 vs. Control group

Article Snippet: Serum concentrations of IL-6 (JL20268, Jonin) and IL-1β (KE10003, Proteintech) were quantified using commercial ELISA kits according to manufacturers’ protocols.

Techniques: Quantitative RT-PCR, Activity Assay, Control

Journal: BMC Gastroenterology

Article Title: Inhibition of TLR4 enhances oxaliplatin chemotherapy sensitivity in esophageal squamous cell carcinoma by suppressing inflammation and glycolysis

doi: 10.1186/s12876-026-04663-2

Figure Lengend Snippet: TLR4 knockout enhances the sensitivity of OXA chemotherapy in ESCC in vivo. A . Number of tumors. B . HE staining of esophageal epithelial tissues. Scale bar: 50 μm. C . Body weight of mice. D , E . the levels of serum IL-1β and IL-6 in mice from different groups were detected by ELISA. F . The immunohistochemical activities of PCNA, CK14, Cyclin D1, COX-2, S100A8 and S100A9 in the esophageal tissue were detected. Scale bar: 100 μm. G , H . The mRNA levels of inflammatory cytokines and glycolysis-related proteins in esophageal tissue were detected by qRT-PCR. * p < 0.05, ** p < 0.01, *** p < 0.001 vs. WT group; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. WT + 4NQO + OXA group

Article Snippet: Serum concentrations of IL-6 (JL20268, Jonin) and IL-1β (KE10003, Proteintech) were quantified using commercial ELISA kits according to manufacturers’ protocols.

Techniques: Knock-Out, In Vivo, Staining, Enzyme-linked Immunosorbent Assay, Immunohistochemical staining, Quantitative RT-PCR

Journal: BMC Gastroenterology

Article Title: Inhibition of TLR4 enhances oxaliplatin chemotherapy sensitivity in esophageal squamous cell carcinoma by suppressing inflammation and glycolysis

doi: 10.1186/s12876-026-04663-2

Figure Lengend Snippet: Schematic diagram illustrating the mechanism by which TLR4 inhibition enhances oxaliplatin (OXA) chemosensitivity in esophageal squamous cell carcinoma (ESCC). OXA treatment upregulates TLR4 and its downstream adaptor protein MYD88, which activates the phosphorylation of NF-κB p65. This activation drives two parallel pathways: (1) the inflammatory response, characterized by the upregulation of pro-inflammatory factors such as IL-6, COX-2, and CXCL5; (2) the glycolytic metabolic reprogramming, mediated by the HIF-1α/GLUT1 axis and enhanced expression of glycolytic enzymes including PFKM and LDHB. These two pathways synergistically promote ESCC cell proliferation, migration, and invasion, ultimately reducing OXA chemosensitivity. Inhibition of TLR4 (via genetic knockout, shRNA knockdown, or pharmacological inhibitor TAK-242) or its downstream mediator MYD88 (via shRNA knockdown or inhibitor ST2825) blocks NF-κB p65 phosphorylation, thereby suppressing both the inflammatory response and glycolytic activity. This dual inhibition disrupts the adaptive survival mechanisms of ESCC cells, potentiating the anti-tumor efficacy of OXA

Article Snippet: Serum concentrations of IL-6 (JL20268, Jonin) and IL-1β (KE10003, Proteintech) were quantified using commercial ELISA kits according to manufacturers’ protocols.

Techniques: Inhibition, Phospho-proteomics, Activation Assay, Expressing, Migration, Knock-Out, shRNA, Knockdown, Activity Assay

Journal: Experimental & Molecular Medicine

Article Title: Local delivery of OSK factors enables partial cellular reprogramming to mitigate osteoarthritis and cartilage fibrosis

doi: 10.1038/s12276-026-01662-x

Figure Lengend Snippet: a , b RT–qPCR analysis of Oct4 , Sox2 , klf4 and c-Myc ( a ) and Sox9 , Nanog ( b ) in primary chondrocytes receiving either AAV-Mock or AAV-OSK treatments. n = 3 per group. c RT–qPCR analysis of inflammatory genes ( Tnf , Il-1α and Il-1β ) and metabolic genes ( Acan , Col2 and Mmp13 ) in ATDC5 cell line under inflammatory environment induced by IL-1β for 24 h, after treatment with vehicle, AAV-Mock or AAV-OSK for 3 days. n = 3 per group. d , e ICC staining of SOX2 and IL-1β in ATDC5 cells under inflammatory conditions and different treatments ( d ) and the percentage of IL-1β positive cells ( e ). n = 3 per group. Scale bar, 50 μm. f Flow cytometry assay of apoptosis in ATDC5 cells induced by TNF, treated with vehicle, AAV-Mock or AAV-OSK. g Quantification of the ratios of apoptotic (Annexin V + /PI + ) cells in f . n = 3 per group. Data are presented as mean ± s.d. and analyzed using one-way ANOVA with Bonferroni post hoc test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: To simulate the inflammatory infiltration observed in OA conditions, ATDC5 cells were exposed to 10 ng/ml interleukin-1β (IL-1β) recombinant protein (Ag23461, Proteintech).

Techniques: Quantitative RT-PCR, Staining, Flow Cytometry

Journal: Oncotarget

Article Title: Upregulation of calprotectin in mild IgE-mediated ovalbumin hypersensitivity

doi: 10.18632/oncotarget.16954

Figure Lengend Snippet: Body weight ( A ) and length ( B ) were monitored weekly from the beginning of the study to the end. There was no significant difference between two groups from days 7 to days 42 (day 7 to 35, n = 5/group; day 42, n = 15/group, P all > 0.05).

Article Snippet: Immunohistochemistry was performed using standard protocols with the following antibodies: IL-1β, (1:100, both from Origene, Inc., Rockville, MD, USA); TNF-α, S100A8, S100A9 (1:200, Abcam, Inc., Cambridge, MA, USA); Toll-like receptor 4 (TLR4), S100A8/A9 (1:200, NOVUSbio, Inc., Littleton, CO, USA); nuclear factor kappa B (NF-κB) (1:200, Cell Signaling Technology, Inc., Danvers, MA, USA).

Techniques:

Journal: Oncotarget

Article Title: Upregulation of calprotectin in mild IgE-mediated ovalbumin hypersensitivity

doi: 10.18632/oncotarget.16954

Figure Lengend Snippet: PCR was used to detect the mRNA expression of TLR4, NF-κB, TNF-α, IL-1β, and IL-6. ( A , B , C , D , and E ) show the expression of TLR4, NF-κB, TNF-α, IL-1β, and IL-6 in jejunum; ( F , G , H , I and J ) show the expression of TLR4, NF-κB, TNF-α, IL-1β, and IL-6 mRNA in liver. * P < 0.05 ; # P < 0.01. ( K ) shows the expression of TLR4, NF-κB, TNF-α, and IL-1β. from left to right are control group, hypersensitivity groups from day 7 to day 42; and from top to bottom, expression of TLR4, NF-κB, TNF-α, and IL-1β in jejunum.

Article Snippet: Immunohistochemistry was performed using standard protocols with the following antibodies: IL-1β, (1:100, both from Origene, Inc., Rockville, MD, USA); TNF-α, S100A8, S100A9 (1:200, Abcam, Inc., Cambridge, MA, USA); Toll-like receptor 4 (TLR4), S100A8/A9 (1:200, NOVUSbio, Inc., Littleton, CO, USA); nuclear factor kappa B (NF-κB) (1:200, Cell Signaling Technology, Inc., Danvers, MA, USA).

Techniques: Expressing, Control

Journal:

Article Title: High-Level Replication of Human Immunodeficiency Virus in Thymocytes Requires NF-?B Activation through Interaction with Thymic Epithelial Cells

doi:

Figure Lengend Snippet: TNF and, to a lesser extent, IL-1 are involved in the permanently induced NF-κB activity present in thymocytes during the coculture with TEC. Thymocytes were freshly isolated (lanes 1 and 2) or cultured for 45 h (lanes 3 to 11) either alone (lane 3 [Control thymocytes]) or in the presence of TEC under conditions avoiding contact (lanes 4 to 9) or allowing contact (lanes 10 and 11). During the coculture, the cells were either left untreated (lane 4 [Control coculture, 45 hours] and lane 10 [Control coculture]) or were treated at the start of the coculture with antibodies respectively raised against TNF (lane 5), IL-6 (lane 6), and IL-1β (lane 8), with the antagonist of the IL-1 receptor (lane 7), or with αTNF plus IL-1 ra plus αIL-6 (lanes 9 and 11). Whole-cell extracts from these various samples were incubated with a 32P-labeled oligonucleotide representing the HIV LTR-derived κB motif. Competition (comp [lane 1]) with a 40-fold molar excess of unlabeled oligonucleotide was used to confirm the specificity of the DNA-binding activity detected. NF-κB activity is indicated. The positions of two nonspecific (n.s 1 and n.s 2) binding activities are indicated. The positions of two nonspecific (n.s 1 and n.s 2) binding activities are indicated. This experiment is representative of three independent experiments, each carried out on a different thymus.

Article Snippet: MAb against IL-1β (B-A15) was purchased from Diaclone Research (Besançon, France).

Techniques: Activity Assay, Isolation, Cell Culture, Incubation, Labeling, Derivative Assay, Binding Assay

Journal:

Article Title: High-Level Replication of Human Immunodeficiency Virus in Thymocytes Requires NF-?B Activation through Interaction with Thymic Epithelial Cells

doi:

Figure Lengend Snippet: TNF and, to a lesser extent, IL-1 induce NF-κB activity in thymocytes, and IL-7 is required for this effect. Whole-cell extracts were prepared from freshly isolated thymocytes (panel A, lane 1) or from thymocytes cultivated for 30, 60, or 45 h. (A) During the indicated culture times, thymocytes were either left untreated (lane 1, control for freshly isolated; lane 2, control 30 h; and lane 5, control 60 h) or were stimulated with either TNF (lanes 3 and 6), IL-1β (lanes 4 and 7), or TNF in the presence of TEC CM (TEC CM + TNF) (lane 9). TEC conditioned medium was also added alone (lane 8 [TEC CM]). The data shown here are representative of three independent experiments carried out on three thymuses. (B) Thymocytes were cultured for 45 h either untreated (lane 1, control 45 h), with TNF (lane 2), with TEC CM (lane 3), or with TNF in the presence of TEC CM (TEC CM + TNF) preincubated (lane 5) or not (lane 4) with antibody against IL-7. In lanes 6 to 8, the thymocytes were left untreated for 6 h (lane 6) or incubated with an antibody against IL-7Rα (lane 7) or with an IgG1 control serum (lane 8) before being cocultured with TEC for 45 h. The data shown here are representative of two independent experiments carried out on two thymuses. (C) Cells were left untreated for the 45 h of the culture (lane 1, control 45 h) or treated with IL-1β (lane 2), TNF (lane 3), IL-1β plus TNF plus IL-6 plus GM-CSF (lane 4), IL-7 (lane 5), IL-7 plus IL-1β (lane 6), or IL-7 plus TNF (lane 7). This experiment is representative of three independent experiments carried out on three thymuses. (D) Thymocytes were left untreated (lane 1, control) or stimulated with IL-7 (lane 2) or IL-7 in presence of anti-TNF and Il-1ra (lane 3). Whole-cell extracts were incubated with a 32P-labeled oligonucleotide representing κB motif. NF-κB activity is indicated. This experiment is representative of two independent experiments, each carried out on a different thymus.

Article Snippet: MAb against IL-1β (B-A15) was purchased from Diaclone Research (Besançon, France).

Techniques: Activity Assay, Isolation, Cell Culture, Incubation, Labeling