Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from footpad of AIRmax and AIRmin mice submitted to pristane arthritis induction

ABSTRACT: Mice selected for high and low acute inflammation were tested for pristane induced arthritis, showing to be susceptible and resistant, respectively. We used microarrays to detail the global programme of gene expression underlying arthritis progression during induction and identified distinct classes of differentially expressed genes during this process in the footpad of these mice. AIRmax (high inflammation) and AIRmin (low inflammation) mouse footpads were collected for RNA extraction and hybridization on Affymetrix microarrays. We compared control and experimental footpads from male and female AIRmax and AIRmin mice on days 0 and 160, respectively. Please note that the AIRmax and AIRmin mice were obtained through bidirectional genetic selection, starting with a genetically heterogeneous founder population (F0) produced by intercrossing eight isogenic strains of mice of independent origins (A/J, DBA/2J, P/J, SWR/J, SJL/J, CBA/J, BALB/cJ and C57BL/6J).

ORGANISM(S): Mus musculus

SUBMITTER: Marcelo De Franco

PROVIDER: E-GEOD-51516 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Background: Prenatal alcohol exposure (PAE) is associated with alterations in numerous physiological systems, including the stress and immune systems. We have previously shown that PAE increases the course and severity of arthritis in an adjuvant-induced arthritis (AA) model. While the molecular mechanisms underlying these effects are not fully known, changes in neural gene expression are emerging as important factors in the etiology of PAE effects. As the prefrontal cortex (PFC) and hippocampus (HPC) play key roles in neuroimmune function, PAE-induced alterations to their transcriptome may underlie abnormal steady-state functions and responses to immune challenge. The current study examined brains from adult PAE and control females from our recent AA study to determine whether PAE causes long-term alterations in gene expression and whether these mediate the altered severity and course of arthritis in PAE females Methods: Adult females from PAE, pair-fed [PF], and ad libitum-fed control [C]) groups were injected with either saline or complete FreundM-bM-^@M-^Ys adjuvant. Animals were terminated at the peak of inflammation or during resolution (days 16 and 39 post-injection, respectively); cohorts of saline-injected PAE, PF and C females were terminated in parallel. Gene expression was analyzed in the PFC and HPC using whole genome mRNA expression microarrays. Results: Significant changes in gene expression in both the PFC and HPC were found in PAE compared to controls in response to ethanol exposure alone (saline-injected females), including genes involved in neurodevelopment, apoptosis, and energy metabolism. Moreover, in response to inflammation (adjuvant-injected females), PAE animals showed unique expression patterns, while failing to exhibit the activation of genes and regulators involved in the immune response observed in control and pair-fed animals. Conclusions: These results support the hypothesis that PAE affects neuroimmune function at the level of gene expression, demonstrating long-term effects of PAE on the CNS response under steady-state conditions and following an inflammatory insult. Key words: prenatal alcohol exposure (PAE), ethanol, inflammation, arthritis, gene expression, rat. 192 samples, including 20 hybridization replicates

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Expression data from footpad of AIRmax and AIRmin mice submitted to pristane arthritis induction

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