LPS response during systemic infection
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ABSTRACT:
PROVIDER: PRJNA378232 | ENA |
REPOSITORIES: ENA
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Project description:The overall study examines the mechanism and role of innate re-stimulation of T cells after activation and differentiation during infection. This particular study is focused on the restimulation of Th1 cells activated during Chlamydia infection, using in vivo LPS stimulation to increase the response. The study was conducted to compare the expression profile after LPS stimulation during Chlamydia infection to that seen after LPS stimulation during Salmonella infection (submitted as a separate dataset).
2017-03-07 | GSE95725 | GEO
Project description:We studied the response to infection and associated perturbations to the bovine liver’s normal function by examining gene transcription data from liver biopsies collected following an E. coli infection in the udder of primiparous dairy cows. This is the first study to examine gene transcription responses to systemic infection by the E. coli bacterium in dairy cows. First, we verified that the inoculation protocol resulted in systemic infection in the cows. This was done based on records on three clinical symptoms: body temperature and amount of E. coli bacteria and leukocytes in milk samples. Second, we examined gene transcription patterns underlying the clinical traits. Gene transcription levels at times of peak values for the clinical traits were estimated in the liver to study indications of an acute phase response to systemic E. coli infection in the cows. Finally, we compared gene transcription responses to E. coli infection and lipopolysaccaride (LPS) inoculation. Sixteen healthy, primiparous Danish Holstein-Friesian cows were challenged intramammarily with E. coli 4 to 6 weeks following parturition. Gene transcription levels for fifteen of the cows were used to study infection responses. We compared gene transcription levels before and after E. coli infection for all fourteen cows.
2012-01-01 | E-GEOD-25319 | biostudies-arrayexpress
Project description:LPS response during systemic Chlamydia infection
| PRJNA378227 | ENA
Project description:We studied the response to infection and associated perturbations to the bovine liver’s normal function by examining gene transcription data from liver biopsies collected following an E. coli infection in the udder of primiparous dairy cows. This is the first study to examine gene transcription responses to systemic infection by the E. coli bacterium in dairy cows. First, we verified that the inoculation protocol resulted in systemic infection in the cows. This was done based on records on three clinical symptoms: body temperature and amount of E. coli bacteria and leukocytes in milk samples. Second, we examined gene transcription patterns underlying the clinical traits. Gene transcription levels at times of peak values for the clinical traits were estimated in the liver to study indications of an acute phase response to systemic E. coli infection in the cows. Finally, we compared gene transcription responses to E. coli infection and lipopolysaccaride (LPS) inoculation.
2012-01-01 | GSE25319 | GEO
Project description:Our recent study of gene expression in mice treated with LPS systemically identified the E2F1 transcription factor as a novel regulator of innate immune response in lung, liver, and spleen tissue. Our follow up studies showed that RNAi-mediated inhibition or E2F1 gene deficiency lead to reduced inflammatory response to LPS in vitro and in vivo. Furthermore, a clear role for the role of miRNAs in the regulation of innate immune response to LPS has emerged. In the current study, we further examined B6;129E2F1-/- and B6x126 F2 mice in the systemic LPS model and used gene expression profiling to identify a defect in the coagulation cascade that contributes to increased morbidity of B6;129E2F1-/- mice despite their reduced systemic inflammatory response. We also studied miRNA expression profiles identified miRNAs that are differentially expressed in B6;129E2F1-/- but not B6x129 F2 mice. 32 mice (4-6) per group, E2F+/+ or E2F-/- genotype, treated with saline or LPS, 6 or 20 hrs
2012-06-30 | E-GEOD-33901 | biostudies-arrayexpress
Project description:Our recent study of gene expression in mice treated with LPS systemically identified the E2F1 transcription factor as a novel regulator of innate immune response in lung, liver, and spleen tissue. Our follow up studies showed that RNAi-mediated inhibition or E2F1 gene deficiency lead to reduced inflammatory response to LPS in vitro and in vivo. Furthermore, a clear role for the role of miRNAs in the regulation of innate immune response to LPS has emerged. In the current study, we further examined B6;129E2F1-/- and B6x126 F2 mice in the systemic LPS model and used gene expression profiling to identify a defect in the coagulation cascade that contributes to increased morbidity of B6;129E2F1-/- mice despite their reduced systemic inflammatory response. We also studied miRNA expression profiles identified miRNAs that are differentially expressed in B6;129E2F1-/- but not B6x129 F2 mice. 32 mice (4-6) per group, E2F+/+ or E2F-/- genotype, treated with saline or LPS, 6 or 20 hrs
2012-06-30 | E-GEOD-33900 | biostudies-arrayexpress
Project description:Background: Our understanding of the role host genetic factors play in the initiation and severity of infections caused by Gram negative bacteria is incomplete. Methods: To identify novel regulators of the host response to lipopolysaccharide (LPS), 11 inbred murine strains were challenged with LPS systemically. RNA from lung, liver, and spleen tissue was profiled on oligonucleotide microarrays to determine if unique transcripts differentiate susceptible and resistant strains of mice. Gene expression data were analyzed to identify over-represented pathways and transcription factors (TFs). The role of several TFs in innate immune response to LPS was examined by RNA interference in a mouse macrophage cell line. Mouse lines with targeted mutations were utilized to further confirm involvement of two novel genes in innate immunity. Results: In addition to two strains lacking functional TLR4 (C3H/HeJ and C57BL/6JTLR4-/-), three murine strains with functional TLR4 (C57BL/6, 129/SvlmJ, and NZW/LacJ) were found to be resistant to systemic LPS challenge; the other six strains were classified as sensitive. Gene expression analysis supports the involvement of a number of previously identified genes, molecular pathways, and TFs in the host response to LPS but also identifies Hedgehog signaling as a novel pathway activated by LPS. B6;129Ptch1+/+ wild-type mice were shown to be more sensitive to systemic LPS than B6;129Ptch1+/- heterozygote littermates further supporting the role of Hedgehog signaling in systemic LPS response. RNA interference-mediated inhibition of 6 TFs (C/EBP, Cdx-2, E2F1, Hoxa4, Nhlh1, and Tead2), out of 15 tested, was found to diminish production of IL-6 and TNF protein in murine macrophages. The role of E2F1 was confirmed by showing that B6;129E2F1-/- knockout mice are more sensitive to systemic LPS than wild-type controls. Conclusions: Our analysis of gene expression data identified novel pathways and transcription factors that regulate the host response to systemic LPS. Our results provide potential sepsis biomarkers and therapeutic targets that should be further investigated in human populations. Keywords: disease state analysis For each strain of mice, 6 mice were treated with LPS and 6 with saline. RNA of 3 animals was pooled to make two pools per condition (two biological replicates). Each pool was labeled with Cy3 and Cy5 and co-hybridized with Stratagene Univeral Mouse Reference (dye flip techical replicates). RNA from lung, liver, and spleen tissue was profiled on oligonucleotide microarrays
2009-07-01 | E-GEOD-14675 | biostudies-arrayexpress
Project description:Background: Our understanding of the role host genetic factors play in the initiation and severity of infections caused by Gram negative bacteria is incomplete. Methods: To identify novel regulators of the host response to lipopolysaccharide (LPS), 11 inbred murine strains were challenged with LPS systemically. RNA from lung, liver, and spleen tissue was profiled on oligonucleotide microarrays to determine if unique transcripts differentiate susceptible and resistant strains of mice. Gene expression data were analyzed to identify over-represented pathways and transcription factors (TFs). The role of several TFs in innate immune response to LPS was examined by RNA interference in a mouse macrophage cell line. Mouse lines with targeted mutations were utilized to further confirm involvement of two novel genes in innate immunity. Results: In addition to two strains lacking functional TLR4 (C3H/HeJ and C57BL/6JTLR4-/-), three murine strains with functional TLR4 (C57BL/6, 129/SvlmJ, and NZW/LacJ) were found to be resistant to systemic LPS challenge; the other six strains were classified as sensitive. Gene expression analysis supports the involvement of a number of previously identified genes, molecular pathways, and TFs in the host response to LPS but also identifies Hedgehog signaling as a novel pathway activated by LPS. B6;129Ptch1+/+ wild-type mice were shown to be more sensitive to systemic LPS than B6;129Ptch1+/- heterozygote littermates further supporting the role of Hedgehog signaling in systemic LPS response. RNA interference-mediated inhibition of 6 TFs (C/EBP, Cdx-2, E2F1, Hoxa4, Nhlh1, and Tead2), out of 15 tested, was found to diminish production of IL-6 and TNFalpha protein in murine macrophages. The role of E2F1 was confirmed by showing that B6;129E2F1-/- knockout mice are more sensitive to systemic LPS than wild-type controls. Conclusions: Our analysis of gene expression data identified novel pathways and transcription factors that regulate the host response to systemic LPS. Our results provide potential sepsis biomarkers and therapeutic targets that should be further investigated in human populations. Keywords: disease state analysis
2009-07-01 | GSE14675 | GEO
Project description:Our recent study of gene expression in mice treated with LPS systemically identified the E2F1 transcription factor as a novel regulator of innate immune response in lung, liver, and spleen tissue. Our follow up studies showed that RNAi-mediated inhibition or E2F1 gene deficiency lead to reduced inflammatory response to LPS in vitro and in vivo. Furthermore, a clear role for the role of miRNAs in the regulation of innate immune response to LPS has emerged. In the current study, we further examined B6;129E2F1-/- and B6x126 F2 mice in the systemic LPS model and used gene expression profiling to identify a defect in the coagulation cascade that contributes to increased morbidity of B6;129E2F1-/- mice despite their reduced systemic inflammatory response. We also studied miRNA expression profiles identified miRNAs that are differentially expressed in B6;129E2F1-/- but not B6x129 F2 mice.
2012-07-01 | GSE33901 | GEO
Project description:Our recent study of gene expression in mice treated with LPS systemically identified the E2F1 transcription factor as a novel regulator of innate immune response in lung, liver, and spleen tissue. Our follow up studies showed that RNAi-mediated inhibition or E2F1 gene deficiency lead to reduced inflammatory response to LPS in vitro and in vivo. Furthermore, a clear role for the role of miRNAs in the regulation of innate immune response to LPS has emerged. In the current study, we further examined B6;129E2F1-/- and B6x126 F2 mice in the systemic LPS model and used gene expression profiling to identify a defect in the coagulation cascade that contributes to increased morbidity of B6;129E2F1-/- mice despite their reduced systemic inflammatory response. We also studied miRNA expression profiles identified miRNAs that are differentially expressed in B6;129E2F1-/- but not B6x129 F2 mice.
2012-07-01 | GSE33900 | GEO