Protein microarray analysis of expression of murine cytokines in spleen interfered with IFN-α and (or) LPS
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE42183 | GEO | 2012/11/10
SECONDARY ACCESSION(S): PRJNA179242
REPOSITORIES: GEO
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Project description:12 wild-type C57BL/6 (B6) mice were divided into 4 groups: control group, IFN-α group, LPS group, and IFN-α+ LPS group, every group contained 3 mice (n=3). IFN-α was administrated i.p. to IFN-α group and IFN-α+ LPS group once daily (QD) for 7 days at a medium dose of 105units/kg weight, PBS was administrated i.p. to control group and LPS group QD for 7 days at the same volume. LPS group and IFN-α+ LPS group were injected i.v. with 10 μg LPS for one mouse on the 8th day. Control group and IFN-α group were injected i.v. with PBS at the same volume. 6 h later, mice were sacrificed to harvest spleens for protein microarray experiment. Mouse Cytokine Antibody Array 3(62) was purchased from Ray Biotech, Norcross GA, US. Protein microarray of murine cytokines expression. Spleens from 12 mice (4 group) were treated as indicated in the summary. Equal amount total protein from each spleen was pooled prior to gene expression analysis.
2012-11-10 | E-GEOD-42183 | biostudies-arrayexpress
Project description:Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an inflammatory process of the lungs characterized by increased permeability of the alveolar-capillary membrane with subsequent interstitial/alveolar edema and diffuse alveolar damage. ALI/ARDS can be the results of either direct or indirect lung injury, with pneumonia being the most common direct pulmonary insult and sepsis the most common extra-pulmonary cause. In this study, we employed the murine lipopolysaccharide (LPS)-induced direct and indirect lung injury model to explore the pathogenic mechanisms of pulmonary and extra-pulmonary ARDS, using an unbiased, discovery and quantitative proteomic approach. A total of 1,017 proteins were both identified and quantified in bronchoalveolar lavage fluid (BALF) from control, intratracheal LPS (I.T. LPS, 0.1 mg/kg) and intraperitoneal LPS (I.P. LPS, 5 mg/kg) treated mice. The two LPS groups shared 13 up-regulated and 22 down-regulated proteins compared to the control group. Among them, molecules related to bronchial and type II alveolar epithelial cell functions including cell adhesion molecule 1 and surfactant protein B were reduced, whereas lactotransferrin and resistin like alpha involved in lung innate immunity were upregulated in both LPS groups. Proteomic profiling also identified significant differences in BALF proteins between I.T. and I.P. LPS groups. Ingenuity pathway analysis revealed that acute-phase response signaling was activated by both I.T. and I.P. LPS, however, the magnitude of activation is much greater in I.T. LPS group compared to I.P. LPS group. Intriguingly, two canonical signaling pathways, liver X receptor/retinoid X receptor activation and the production of nitric oxide and reactive oxygen species in macrophages, were activated by I.T. LPS but suppressed by I.P. LPS. In addition, CXCL15 (also known as lungkine) was also up-regulated by I.T LPS but down-regulated by I.P. LPS. In conclusion, our quantitative discovery-based proteomic approach identified commonalities as well as significant differences in BALF protein expression profiles in LPS-induced direct and indirect lung injury, and importantly, LPS-induced indirect lung injury results in suppression of select components of lung innate immunity, which could contribute to the so-called “immunoparalysis” in sepsis patients.
2019-07-11 | PXD014070 | Pride
Project description:The acute phase response is poorly studied in chickens, but its examination can possibly supply valuable markers for the identification of subclinical disease and assessment of disease severity. We therefore injected ten six weeks-old Lohmann Selected Leghorn chickens i.v. with 10µg LPS per kg body weight (n=5) or the same volume of PBS as controls (n=5) and collected spleens after three hours. Spleens were kept in ice cold PBS and RNA was isolated immediately. After quality control of RNA (RIN>9.0), a cDNA library was prepared and submitted to Illumina high-throughput sequencing.
2019-01-18 | E-MTAB-7082 | biostudies-arrayexpress
Project description:Aim: To find the genes that related with the drug's(7-P) function. Design: 36 Rats were randomly divided into three group:control group(12), model group(12) and drug group(12). At last, randomly choosing 3 Rat from each group to do genechip analysis. In model group, the Porcine serum was given intraperitoneally (i.p.) to rats in a volume of 1.5 mL/kg every 3 days for a total of 20 treatments. Effect on model animals was confirmed by liver histology and biochemical assays . In drug group, 7-P was dissolved in balanced saline solution for administration subcutaneously at dosages of 174 μg/kg in a volume of 1 mL/kg. The doses were given 15 times, one day interval. In control group, the animals were not treated with porcine serum. but given an equal volume of vehicle alone. During 7-P and vehicle administration, porcine serum was given intraperitoneally (i.p.) to rats in a volume of 1.5 mL/ kg once weekly. All animals were fasted for 24 h before porcine serum treatment. Background: During investigation of hypervariable region 1 (HVR1) of hepatitis C virus (HCV), a seven amino acids mimic peptide named 7-P was identified within the N-terminal of HVR1 that could induce IFN-γ and IL-10 expression while decreasing the expression of TNF-α in vivo and in vitro. Further studies revealed that 7-P could not only decrease the serum levels of aminotransferases (ALT, AST), alkaline phosphatase (AKP), and billirubin, but were also effective in reversing histopathological evidence of inflammation-mediated hepatic injury in 3 rat models. The protective mechanism and gene expression profiles were investigated in detail in a rat chronic liver injury model using Affymetrix microarrays . Conclusion: We found that IL-1β, tumor necrosis factor receptor superfamily 14 (TNFRSF14), intercellular adhesion molecule 2 (ICAM2), sterol regulatory element-binding protein 1 (SREBP 1), Prohibitin (PHB), and inhibitor of DNA binding 2 (Id2) were the target genes that related with 7-P Keywords: comparative genomic hybridization
2009-09-30 | GSE10669 | GEO
Project description:This study aimed to investigate the protective mechanisms of didymin on acute liver injury,mice were intragastrically administrated with the equal volume of saline or didymin once per day for two weeks.after that,except the normal group, mice were injected with LPS (50 μg/kg) and D-Gal (800 mg/kg) intraperitoneally to induce ALI; Finally, the transcriptomic analysis was performed to acquire the differently expressed genes amog these groups, trying to figure out the potential targets, which regulated by didymin.
2021-12-15 | GSE190823 | GEO
Project description:To examine the effects of GSK199 treatment on antibody responses, a synovial antigen array analysis was performed using day 35 sera derived from mice with CIA treated with 30 mg/kg qd, 30 mg/kg bid GSK199 or saline. The synovial antigen arrays contain nearly 200 peptides and proteins, both citrullinated and uncitrullinated, representing candidate antigens in RA. Significance Analysis of Microarrays identified 7 and 14 autoantibody reactivities that were statistically decreased in CIA mice treated with 30 mg/kg qd or 30 mg/kg bid GSK199 respectively, compared to PBS treatment. By comparison, over 150 native and citrullinated epitopes on the arrays did not exhibit significant differences in reactivity. Sera from mice treated with 30 mg/kg GSK199 qd exhibited decreased IgG reactivity to native epitopes such as peptides from human fibrinogen alpha and beta chains and keratin while sera from mice treated with 30 mg/kg bid GSK199 demonstrated decreased IgG reactivity to native epitopes including collagen IV, heat shock protein 65, peptides from human fibrinogen alpha and beta chains (two of which match those that were decreased in the 30 mg/kg qd group), and vimentin as compared to saline controls (q < 0.1%). Decreased autoantibody reactivity to citrullinated peptides from vimentin and fibromodulin were also observed in sera from mice treated with 30 mg/kg bid GSK199 compared to controls treated with saline (q < 0.1%), but not by GSK199 30 mg/kg qd. There were no differences between treatment with GSK199 or saline alone in the levels of autoantibodies to 38 other citrullinated proteins in the array. These data demonstrated that GSK199 treatment decreases the development of autoantibodies in CIA and impairs epitope spreading to a degree similar to that observed with pan-PAD inhibition.
2015-10-08 | GSE69680 | GEO
Project description:Aim: To find the genes that related with the drug's(7-P) function. Design: 36 Rats were randomly divided into three group:control group(12), model group(12) and drug group(12). At last, randomly choosing 3 Rat from each group to do genechip analysis. In model group, the Porcine serum was given intraperitoneally (i.p.) to rats in a volume of 1.5 mL/kg every 3 days for a total of 20 treatments. Effect on model animals was confirmed by liver histology and biochemical assays . In drug group, 7-P was dissolved in balanced saline solution for administration subcutaneously at dosages of 174 μg/kg in a volume of 1 mL/kg. The doses were given 15 times, one day interval. In control group, the animals were not treated with porcine serum. but given an equal volume of vehicle alone. During 7-P and vehicle administration, porcine serum was given intraperitoneally (i.p.) to rats in a volume of 1.5 mL/ kg once weekly. All animals were fasted for 24 h before porcine serum treatment. Background: During investigation of hypervariable region 1 (HVR1) of hepatitis C virus (HCV), a seven amino acids mimic peptide named 7-P was identified within the N-terminal of HVR1 that could induce IFN-γ and IL-10 expression while decreasing the expression of TNF-α in vivo and in vitro. Further studies revealed that 7-P could not only decrease the serum levels of aminotransferases (ALT, AST), alkaline phosphatase (AKP), and billirubin, but were also effective in reversing histopathological evidence of inflammation-mediated hepatic injury in 3 rat models. The protective mechanism and gene expression profiles were investigated in detail in a rat chronic liver injury model using Affymetrix microarrays . Conclusion: We found that IL-1β, tumor necrosis factor receptor superfamily 14 (TNFRSF14), intercellular adhesion molecule 2 (ICAM2), sterol regulatory element-binding protein 1 (SREBP 1), Prohibitin (PHB), and inhibitor of DNA binding 2 (Id2) were the target genes that related with 7-P Keywords: comparative genomic hybridization 36 Rats were randomly divided into three group:control group(12), model group(12) and drug group(12). At last, randomly choosing 3 Rat from each group to do genechip analysis.
2009-09-30 | E-GEOD-10669 | biostudies-arrayexpress
Project description:Analysis of gene expression in explanted peritoneal macrophages from Aoah -/- and Aoah +/+ mice treated with LPS 21 days prior to harvest. Explanted peritoneal machrophages were challenged with LPS or control (PBS). The study seeks to characterize global gene expression in the state of prolonged LPS tolerance induced in mice lacking the LPS-inactivating enzyme Aoah. Groups of 9 C57BL/6 Aoah+/+ or Aoah-/- mice were given i.p. injections of 10 µg E. coli LPS/mouse. Twenty-one days later (when Aoah-/- mice remain tolerant and Aoah+/+ mice have recovered), peritoneal macrophages were harvested and the yields from three mice were pooled to form 3 samples per group (i.e., three samples of Aoah+/+ and Aoah-/- mice, with each sample comprised of peritoneal macrophages from 3 mice). Next day, cells were challenged with LPS or PBS and whole RNA was isolated 2 hours later and used for microarray experiments.
2012-08-17 | E-GEOD-40154 | biostudies-arrayexpress
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2017-03-20 | E-MTAB-5567 | biostudies-arrayexpress
Project description:Transcription profiling by array was performed on airway wall samples from PBS, LPS, IFN-gamma and LPS+IFN-gamma treated BALB/c mice 12 hr post treatments.
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