Lungs from mice infected with S. pneumoniae and treated with Nemiralisib
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE109941 | GEO | 2018/08/13
REPOSITORIES: GEO
Similar Datasets
Project description:This experiment is an additional experiment to GSE6688. Mouse macrophages (ANA-1 cells) were infected in vitro with C. pneumoniae with a M.O.I. of 10. Twenty two genes were significantly upregulated. Examples of the most upregulated genes in mouse macrophages after C. pneumoniae infection are serum amyloid A3 (saa3), a protein that is mainly produced by activated macrophages during tissue injury or inflammation, MIP-2 (cxcl2) and irg1. Expression levels of all genes induced by C. pneumoniae in macrophages in vitro correlated with the results obtained from infected lungs from wild type mice (GSE6688), suggesting that this cell type participates in host defense in vivo against C. pneumoniae. Keywords: Chlamydia pneumoniae, ANA-1 macrophages, in vitro, infection
2007-03-27 | GSE6690 | GEO
Project description:Total proteome of human THP1 macrophage infected by Klebsiella pneumoniae, , infection
2025-12-15 | PXD072024 |
Project description:Acute respiratory infections (ARI), which generally begin with colonization of the mucosal surfaces of the upper respiratory tract (URT), are a leading cause of morbidity and mortality with the highest rate in infants. As a common colonizer of the URT, and one of the most prevalent causes of life-threatening infections in the pediatric population, Streptococcus pneumoniae (Spn) was used as a model pathogen to investigate the effect of age during URT infection. We used RNA-sequencing to transcriptionally profile and compare the mucosal epithelia of infant and adult mice at baseline (mock-infected) and during Spn infection. Analysis of the screen revealed an age-dependent alteration of genes involved in mucosal defense mechanisms that included dampened expression of ubiquitous antimicrobial molecules and tight junction proteins in infant mice compared to adults. These results demonstrate a window of vulnerability during postnatal development when altered mucosal barrier function may facilitate bacterial colonization and invasion.
2018-10-16 | GSE116604 | GEO
Project description:Initial transcriptional response of human peripheral monocytes infected with a set of three gram-positive bacterial pathogens (Listeria monocytogenes, Staphylococcus aureus and Streptococcus pneumoniae). Monocytes were isolated from five probands.
2008-12-08 | E-MEXP-1613 | biostudies-arrayexpress
Project description:Lungs from mice infected with S. pneumoniae and treated with Nemiralisib
| PRJNA432397 | ENA
Project description:Bacterial infections of wounds are associated with poor healing and worse scarring. We sought to identify transcriptomic patterns associated with impaired healing of wounds infected with Klebsiella pneumoniae (K.p.) or Pseudomonas aeruginosa (P.a.) using a rabbit ear wound model. Wounds created on post-operative day (POD) 0 were infected on POD3, within the inflammatory phase of healing. On POD4 the infected wounds were harvested for microarray/transcriptome analysis. Other wounds with 24-hour infections were treated with topical antibiotic to promote biofilm formation and harvested on POD6 or POD12. On POD4 before antibiotic treatment, both wounds contained elevated transcripts that enriched predominantly into inflammation/infection-response pathways and functions characteristic of infiltrating leukocytes. But there were 5-fold more elevated transcripts in P.a.- than K.p.-infected wounds. Additionally, unique to P.a.-infected wounds, was a minor network of inflammation/infection-response molecules with predicted upstream regulation predominated by type I interferons. Also on POD4, Dnr-transcripts of both wounds were enriched into stress-response pathways such as EIF2 signaling. But there were 8-fold more Dnr-transcripts in P.a.- than K.p.-infected wounds, and many more of them enriched in the function, cell death, suggesting that resident dermal cells of P.a.-infected wounds failed to survive a more destructive P.a. infection. On POD6, following two days of antibiotic treatment, the biofilm-colonized wounds expressed magnitudes fewer inflammation and stress-response transcripts. However, a single regulatory network of P.a.-infected wounds was found to consist of Upr-transcripts enriching immune/infection-response functions predicted to be regulated by type I interferons, which was similar to the network unique to P.a.-infected wounds on POD4. On POD12, genes expressed by K.p.-infected wounds suggesting healing, while for P.a.-infected wounds they suggested stalled healing. The similarities and differences between the wound responses to these infections further define the molecular foundations of healing impaired by infections. Rabbit ear Wounds created on post-operative day (POD) 0 were infected with Klebsiella pneumoniae (K.p.) or Pseudomonas aeruginosa (P.a.) on POD3 and harvested on POD4 for RNA extraction. Other wounds with 24-hour infections were treated with topical antibiotic to promote biofilm formation and harvested on POD6 or POD12.
2014-01-01 | E-GEOD-51167 | biostudies-arrayexpress
Project description:Purpose:Investigated transcriptome profile changes in the lungs of infected mice at different time points, to increase our understanding of hvKp pulmonary infection and to screen for genes or targets of research value. microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Methods: Animals were randomly divided into four infection groups and one control group (five mice per group), and the infected mice were euthanized at 12, 24, 48 and 60 h post-infection (hpi), respectively, while the control group mice were euthanized immediately after delivery of PBS at the 0 h time point. The lungs of the mice were isolated and divided into two parts for subsequent histopathologic examination or total RNA extraction. Results: Using the control group (0 hpi) as a reference, 6247 DEGs were identified across four time points after hvKp infection. At 12 hpi, 939 upregulated DEGs and 439 downregulated DEGs were detected, and by 60 hpi, 2647 upregulated DEGs and 2806 downregulated DEGs were detected. Overall, the number of upregulated and downregulated DEGs increased over time and a total of 688 genes were upregulated and 240 genes downregulated in common for all time points. And 12 of these were validated with qRT–PCR. RNA-seq data had a linear relationship with qRT–PCR for more than four orders of magnitude and a goodness of fit (R2) of 0.9548. To get a more holistic view, DEGs were clustered into nine clusters according to their temporal expression patterns.WGCNA was performed with the detected DEGs. The dynamic tree cutting algorithm in the WGCNA package was used to process the hierarchical clustering tree, and a total of 28 different modules were finally obtained. Conclusions: Our work both validates the results of previous studies on K. pneumoniae pulmonary infections and provides new additions and insights on hvKp pulmonary infections, which may contribute to the development of therapeutic approaches to reduce hvKp lung inflammation.
2022-03-31 | GSE199546 | GEO
Project description:This experiment is an additional experiment to GSE6688. Mouse macrophages (ANA-1 cells) were infected in vitro with C. pneumoniae with a M.O.I. of 10. Twenty two genes were significantly upregulated. Examples of the most upregulated genes in mouse macrophages after C. pneumoniae infection are serum amyloid A3 (saa3), a protein that is mainly produced by activated macrophages during tissue injury or inflammation, MIP-2 (cxcl2) and irg1. Expression levels of all genes induced by C. pneumoniae in macrophages in vitro correlated with the results obtained from infected lungs from wild type mice (GSE6688), suggesting that this cell type participates in host defense in vivo against C. pneumoniae. Experiment Overall Design: ANA-1 macrophages were infected with Chlamydia pneumoniae or left untreated. After 8h total RNA was extracted. Two biological replicates were performed resulting in 4 arrays in total
2008-06-15 | E-GEOD-6690 | biostudies-arrayexpress
Project description:An infection with SARS-CoV-2 can be symptomatic or asymptomatic depending on the respective activation of the immune system. We used the bacterial extract Broncho Vaxom (BV) to preactivate the immune system before a coronavirus infection using the murine coronavirus MHV A59 in a mouse model. The activation of the immune system led to a reduction in viral load and protected lung tissue from enhanced cell apoptosis. Using RNA sequencing we were able to demonstrate that lung tissue from mice receiving BV resembled an intermediate state between infected and healthy tissue. On a cellular level, treatment with BV enhanced alveolar and interstitial macrophages in the lung. We were able to phenocopy the effect of BV by transplanting naïve lung macrophages into recipient mice thereby enhancing the local cellular amount before infection. We conclude that recruitment and preactivation of the innate immune system by the bacterial extract BV is beneficial during a coronavirus infection.
2021-12-30 | GSE167749 | GEO
Project description:Streptococcus pneumoniae is the primary cause of community-acquired bacterial pneumonia with rates of penicillin and multi-drug resistance exceeding 80% and 40%, respectively. The innate immune response uses various chemical insults to control infection, including metal stress mediated by localized changes in zinc abundance. Here, we characterized the impact of S. pneumoniae zinc intoxication revealing disruptions in central carbon metabolism, lipid biogenesis and peptidoglycan biosynthesis. To dysregulate zinc homeostasis in the wild-type strain, we investigated the safe-for-human use ionophore PBT2. PBT2 rendered wild-type S. pneumoniae strains sensitive to a range of antibiotics.
2021-10-01 | GSE160372 | GEO