Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from infected with Neisseria gonorrhoeae (GC) and uninfected bone marrow derived macrophages from wild type (C67BL/6) and Nod2 knock out mice

ABSTRACT: In this dataset we include the data obtained from 3 hour stimulation with Neisseria gonorrhoeae (GC) of bone marrow macrophages(BMDM) from wild type (C57BL/6) and Nod2 knock out mice (in C57BL/6 background). Murine BMDM from C57BL/6 mice or NOD2 deficient mice on C57BL/6 background, plated in 6 well plates, were infected with GC at MOI 10:1 or left uninfected. At 3 hrs after infection, cells lysates were made and RNA was isolated. All conditions were done in triplicates(3 wells per condition. The experiment was done once). Whole genome microarray analysis was carried out using the Affymetrix GeneChip Gene 1.0 ST Array System. A 2-way ANOVA was applied to analyze the effects of genotype and infection by GC as well as the interaction between genotype and infection by GC. Raw affinity data was normalized using a Robust Multichip Analysis (RMA) method at probe level Microarray Core, Boston University Medical Center

ORGANISM(S): Mus musculus

SUBMITTER: Nikolaos Mavrogiorgos

PROVIDER: E-GEOD-37179 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as CrohnM-bM-^@M-^Ys disease and colorectal cancer. Here, we show that dysbiosis coupled to Nod2 or Rip2 deficiency suffices to cause an increased risk for intestinal inflammation and colitis-associated carcinogenesis in mice. Aggravated epithelial lesions and dysplasia upon chemical-induced injury associated with loss of Nod2 or Rip2 can be prevented by antibiotics or anti-IL6R treatment. Nod2-mediated risk for intestinal inflammation and colitis-associated tumorigenesis is communicable through maternally-transmitted microbiota even to wild-type hosts. Disease progression was identified to drive complex NOD2-dependent changes of the colonic-associated microbiota. Reciprocal microbiota transplantation rescues the vulnerability of Nod2-deficient mice to colonic injury. Altogether, our results unveil an unexpected function for NOD2 in shaping a protective assembly of gut microbial communities, providing a rationale for intentional manipulation of genotype-dependent dysbiosis as a causative therapeutic principle in chronic intestinal inflammation. Analysis used RNA extracted from colonic mucosa of untreated, antibiotics-treated or metronidazole-treated C57Bl/6J and Nod2-deficient mice in CAC model. Direct comparisons were performed as follow: C57Bl/6J untreated mice vs Nod2-deficient untreated mice, C57Bl/6J antibiotics-treated mice vs Nod2-deficient antibiotics-treated mice, C57Bl/6J metronidazole-treated mice vs Nod2-deficient metronidazole-treated mice, C57Bl/6J untreated mice vs C57Bl/6J antibiotics-treated mice, C57Bl/6J untreated mice vs C57Bl/6J metronidazole-treated mice, Nod2-deficient untreated mice vs Nod2-deficient antibiotics-treated mice, Nod2-deficient untreated mice vs Nod2-deficient metronidazole-treated mice. Indirect comparisons with control data were made across multiple arrays with raw data pulled from different channels for data analysis.

Dataset Information

Expression data from infected with Neisseria gonorrhoeae (GC) and uninfected bone marrow derived macrophages from wild type (C67BL/6) and Nod2 knock out mice

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