Journal: Scientific Reports

Article Title: Interferon-β and FTY720 ameliorate progressive CNS inflammation via SOCS1-associated astrocyte signaling

doi: 10.1038/s41598-026-45303-9

Figure Lengend Snippet: Treatment with FTY720 plus IFN-β is associated with a protective glial transcriptional program in astrocytes. Primary murine neonatal astrocytes were treated with vehicle, FTY720 + vehicle, or the combination of FTY720 and IFN-β overnight and subsequently stimulated with IL-1β and TNF-α for 4 h. ( A ) Heatmap of 550 differentially expressed genes in at least two out of the groups (n = 3 biological replicates). ( B ) Heatmap of selected genes differentially expressed in the FTY720 plus IFN-β condition relative to FTY720 alone. ( C ) Ingenuity Pathway Analysis identifying predicted downstream effects in astrocytes treated with FTY720 plus IFN-β compared with FTY720 alone. ( D ) Fold change in mRNA expression of the indicated genes, shown as log2 (combined/FTY720). ( E ) Measurement of Socs1 in activated astrocytes (n = 5 biological replicates). A p-value of p < 0.05 was considered significant and determined by one-way ANOVA followed by Tukey´s multiple-comparisons test. ( F ) Activated primary murine astrocytes were pre- treated with a SOCS1 inhibitor (pJAK2(1001–1013); 20 µM) or a control peptide (20 µM) at the beginning of the pre-treatment phase and maintained throughout cytokine stimulation with IL-1β (10 ng/mL) and TNF-α (5 ng/mL) for 4 h. qPCR was performed for indicated genes (n = 3 biological replicates). ( G ) Activated primary murine astrocytes were treated with FTY720/IFN-β and a control peptide or pJak2(1001–1013). qPCR was performed for indicated genes (n = 3 biological replicates). ( H ) Astrocyte-conditioned medium (ACM) was generated by activating primary astrocytes with IL-1β (10 ng/mL) and TNF-α (5 ng/mL) for 24 h, followed by treatment with FTY720/IFN-β and either the control peptide or pJAK2(1001–1013) (20 µM). The medium was replaced the next day and collected after an additional 24 h. The harvested ACM was added to the lower chamber of a transwell system, and 200,000 isolated monocytes were seeded into the upper insert for a 3 h migration assay. ( I ) Number of migrated monocytes was counted after 3 h. P-values of p < 0.05 were considered significant and determined by Student´s t-test.

Article Snippet: Relative expression levels were then calculated using the ΔΔCt method and are presented as fold change compared to the vehicle-treated control group, which was set to 1.The following TaqMan probes for qPCR were all purchased at Applied Biosystems: Gapdh , Mm99999915_g1; Nos2 , Mm00440502_m1; Csf2 , Mm01290062_m1; Ccl2 , Mm00441242_m1; Tnf-α , Mm00443258_m1; Il-1β , Mm00487229_m1; Vegfb, Mm00442102_m1; Socs1 , Mm00782550_s1; Bdnf, Mm04230607_s1; Ngf , Mm0043039_m1; Lif , Mm00434762_g1; Hbegf , Mm00439306_m1; NGF , Hs00171458_m1; LIF , Hs01055668_m1; HBEGF , Hs00181813_m1.

Techniques: Expressing, Control, Generated, Isolation, Migration

Journal: Viruses

Article Title: UV Light Inhibited HRV1b Replication but Reduced Adherens Epithelial Junction and Antiviral Responses via SOCS1 in Human Respiratory Epithelial Cells

doi: 10.3390/v18030303

Figure Lengend Snippet: IR treatment shows low induction of antiviral response in lung carcinoma epithelial cell line A549 at 48 h. ( a ) Schematic illustration of RV1B infection in the viral recognition capability and antiviral response of airway epithelial cells. ( b ) Effects of viral sensing capability in untreated and IR-irradiated RV-infected A549 epithelial cells measured within 48 h. Data represents six independent repeats per group, representative of two independent experiments. ( c ) Effects of viral recognition in untreated and IR-irradiated RV-infected A549 epithelial cells measured within 72 h. ( d ) Effects of antiviral response in untreated and IR-irradiated RV-infected A549 epithelial cells measured within 48 h. Data represents six independent repeats per group, representative of two independent experiments. ( e ) Effects of antiviral response in untreated and IR-irradiated RV-infected A549 epithelial cells measured within 72 h. ( f ) Schematic illustration of the inhibitory effect of SOCS1 in JAK/STAT pathway in airway epithelial cells after RV1B infection. ( g ) SOCS1 expression in untreated and IR-irradiated RV-infected A549 epithelial cells measured within 48 h. Data represents six independent repeats per group, representative of three independent experiments. ( h ) SOCS1 expression in untreated and IR-irradiated RV-infected A549 epithelial cells measured within 72 h. The mRNA levels of each condition were determined using real-time polymerase chain reaction. Each circular dot represents one independent sample per experiment and the number of dots per group corresponds to the sample size. ( a , f ) Created in BioRender.com.

Article Snippet: The following primers were used ( ): HPRT (hypoxanthine-guanine phosphoribosyl transferase), RPL30 (ribosomal protein L30), RV1B (rhinovirus 1B), ZO-1 (zonulin-1), E-cadherin, TLR3 (toll-like receptor 3), SOCS1 (suppressor of cytokine signaling 1), which were purchased from Eurofins Scientific Group, Luxemburg.

Techniques: Infection, Irradiation, Expressing, Real-time Polymerase Chain Reaction

Journal: Viruses

Article Title: UV Light Inhibited HRV1b Replication but Reduced Adherens Epithelial Junction and Antiviral Responses via SOCS1 in Human Respiratory Epithelial Cells

doi: 10.3390/v18030303

Figure Lengend Snippet: IR 72 h treatment induces antiviral response in RV-infected nasal epithelial cells. ( a ) Schematic illustration of RV1B infection in the viral recognition capability and antiviral response of airway epithelial cells. ( b ) Effects of viral sensing capability in untreated and IR-irradiated RV-infected NECs measured within 72 h. Data represents three patients per group, representative of one independent experiment. ( c ) Effects of antiviral response in untreated and IR-irradiated RV-infected NECs measured within 72 h. Data represents three patients per group, representative of one independent experiment. ( d ) Schematic illustration of the inhibitory effect of SOCS1 in JAK/STAT pathway in airway epithelial cells after RV1B infection. ( e ) SOCS1 expression in untreated RV mRNA and IR-irradiated RV mRNA in NECs measured within 72 h. Data represents three patients per group, representative of one independent experiment. The mRNA levels of each condition were determined using real-time polymerase chain reaction. Each circular dot represents one independent sample per experiment and the number of dots per group corresponds to the sample size. ( a , d ) Created by BioRender.com.

Article Snippet: The following primers were used ( ): HPRT (hypoxanthine-guanine phosphoribosyl transferase), RPL30 (ribosomal protein L30), RV1B (rhinovirus 1B), ZO-1 (zonulin-1), E-cadherin, TLR3 (toll-like receptor 3), SOCS1 (suppressor of cytokine signaling 1), which were purchased from Eurofins Scientific Group, Luxemburg.

Techniques: Infection, Irradiation, Expressing, Real-time Polymerase Chain Reaction

Journal: Viruses

Article Title: UV Light Inhibited HRV1b Replication but Reduced Adherens Epithelial Junction and Antiviral Responses via SOCS1 in Human Respiratory Epithelial Cells

doi: 10.3390/v18030303

Figure Lengend Snippet: UV irradiation eliminated RV1B mRNA in nasal epithelial cells (NECs) but inhibited antiviral responses and cell integrity. ( a ) Experimental design of RV1B infection in NEC culture and UV irradiation. Created in BioRender.com. ( b ) Effects of RV infection in untreated and UV-irradiated RV-infected NECs at 48h. ( c ) Tight junctions in untreated and UV-irradiated RV-infected NECs measured within 48h. Each circular dot represents one independent sample per experiment and the number of dots per group corresponds to the sample size. Data represents three patients per group. ( d ) Expression of adherens junctions in untreated and UV-irradiated RV-infected NECs measured within 48h. Data represents three patients per group. ( e ) Viral sensing capability in untreated and IR-irradiated RV-infected NECs measured within 48 h. ( f ) Effects of antiviral response in untreated and UV-irradiated RV-infected NECs measured within 48h. ( g ) SOCS1 expression in untreated and UV-irradiated RV-infected NECs measured within 48 h. The mRNA levels of each condition were determined using real-time polymerase chain reaction. UV reduced the RV infection and inhibited the antiviral function after UV treatment.

Article Snippet: The following primers were used ( ): HPRT (hypoxanthine-guanine phosphoribosyl transferase), RPL30 (ribosomal protein L30), RV1B (rhinovirus 1B), ZO-1 (zonulin-1), E-cadherin, TLR3 (toll-like receptor 3), SOCS1 (suppressor of cytokine signaling 1), which were purchased from Eurofins Scientific Group, Luxemburg.

Techniques: Irradiation, Infection, Expressing, Real-time Polymerase Chain Reaction

Journal: Viruses

Article Title: UV Light Inhibited HRV1b Replication but Reduced Adherens Epithelial Junction and Antiviral Responses via SOCS1 in Human Respiratory Epithelial Cells

doi: 10.3390/v18030303

Figure Lengend Snippet: UV light induced SOCS1 mRNA in UV-irradiated uninfected tumor epithelial cells while reducing it in the case of RV-infected cells within 72 h. ( a ) Schematic illustration of the inhibitory effect of SOCS1 in the JAK/STAT pathway in airway epithelial cells after RV1B infection. Created in BioRender.com. ( b ) SOCS1 expression in untreated and UV-irradiated RV-infected A549 epithelial cells measured within 48 h. Data represents six independent repeats per group, representative of three independent experiments. ( c ) SOCS1 expression in untreated and UV-irradiated RV-infected A549 epithelial cells measured within 72 h. Data represents three independent repeats per group, representative of one independent experiment. ( d ) Comparison between SOCS1 mRNA expression levels in untreated and UV light post-treated conditions within 48 h and 72 h. The immune responses in RV-infected airway epithelial cells were reduced after UV 72 h treatment, which were higher in uninfected cells. The mRNA levels of each condition were determined using real-time polymerase chain reaction. One-way ANOVA analysis with Tukey’s post hoc test was performed to test statistical significance. p values * p < 0.05; **** p < 0.0001. Each circular dot represents one independent sample per experiment and the number of dots per group corresponds to the sample size.

Article Snippet: The following primers were used ( ): HPRT (hypoxanthine-guanine phosphoribosyl transferase), RPL30 (ribosomal protein L30), RV1B (rhinovirus 1B), ZO-1 (zonulin-1), E-cadherin, TLR3 (toll-like receptor 3), SOCS1 (suppressor of cytokine signaling 1), which were purchased from Eurofins Scientific Group, Luxemburg.

Techniques: Irradiation, Infection, Expressing, Comparison, Real-time Polymerase Chain Reaction