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Profile analysis of circRNAs in osteoblasts infected by Staphylococcus aureus

ABSTRACT: This study aims to compare differential expression circRNA between normal and Staphylococcus aureus infection in osteoblasts

ORGANISM(S): Homo sapiens

PROVIDER: GSE217234 | GEO | 2022/11/08

REPOSITORIES: GEO

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Profile analysis of circRNAs in osteoclasts infected by intracellular Staphylococcus aureus

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Profile analysis of circRNAs in human THP-1 derived macrophages infected with intracellular Staphylococcus aureus

Project description:Background: Intracellular Staphylococcus aureus (S. aureus) infection is generally persistent, recurrent and difficult to treat due to the poor availability of antibiotics within macrophages cells and the lack of ideal diagnostic markers. Circular RNA (circRNA), with covalently closed circular structures, exists in the serum stably and is not easily degraded by nucleases. CircRNAs play important roles in the eukaryotic regulation of genes expression and served as biomarkers in variety disease including infections. However, the function of host circRNAs in intracellular S. aureus infection remains largely unclear. Methods: In this study, an intracellular survival THP-1 derived macrophages model of S. aureus infection was established. Then, the circRNA expression profile was investigated by RNA sequencing technology in both S. aureus -infected THP-1 cells and mock control cells. The differentially expressed (DE) circRNAs with a fold-change ≥2.0 (p<0.05) are analyzed using functional pathway clustering prediction. RT-qPCR was performed to verify the top 9 DE circRNAs. Results: A total of 5,299 circRNAs were detected during the intracellular S. aureus infection. 61 DE circRNAs with a fold-change ≥1.5 (p<0.05) after S. aureus infection were identified. 22 circRNAs were up-regulated while 39 circRNAs were down-regulated. Functional annotation analysis demonstrated that Lysine degradation, RNA degradation and Neurotrophin signaling pathway are most important in intracellular S. aureus infection. Conclusion: Our study provides the first profile analysis of circRNAs involved in intracellular S. aureus infection, which may contribute to the understanding of its host evasion mechanisms.

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Profile analysis of circRNAs in osteoblasts infected by Staphylococcus aureus

Project description:Profile analysis of circRNAs in osteoblasts infected by Staphylococcus aureus

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Caenorhabditis elegans infected with Staphylococcus aureus

Project description:Young adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection. Keywords: response to pathogen infection, innate immunity, host-pathogen interactions

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Transcription profiling of human primary bone cells exposed to Staphylococcus aureus

Project description:Primary human bone derived osteoblasts were employed to examine the cellular responding to Staphylococcus aureus infection in vitro. The transcription profile of host cells was investigated by microarray technology.

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Staphylococcus aureus infection induces the production of the neutrophil chemoattractants CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7 by osteoblasts

Project description:Staphylococcus aureus is the principal causative agent of osteomyelitis, a serious bacterial infection of bone that is associated with progressive inflammatory damage. Bone-forming osteoblasts have increasingly been recognized to play an important role in the initiation and progression of detrimental inflammation at sites of infection, and have been demonstrated to release an array of inflammatory mediators and factors that promote osteoclastogenesis and leukocyte recruitment following bacterial challenge. In the present study, we describe elevated bone tissue levels of the potent neutrophil-attracting chemokines, CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7, in a murine model of post-traumatic staphylococcal osteomyelitis. RNA-Seq gene ontology analysis of isolated primary murine osteoblasts showed enrichment in differentially expressed genes involved in cell migration and chemokine receptor binding and chemokine activity following S. aureus infection, and a rapid increase in the expression of mRNA encoding CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7, in these cells. Importantly, we have confirmed that such upregulated gene expression results in protein production with the demonstration that S. aureus challenge elicits the rapid and robust release of these chemokines by osteoblasts and does so in a bacterial dose-dependent manner. Furthermore, we have confirmed the ability of soluble osteoblast-derived chemoattractants to elicit the migration of a neutrophil-like cell line. As such, these studies demonstrate the robust production of CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7, by osteoblasts in response to S. aureus infection, and the release of such neutrophil-attracting chemokines provides an additional mechanism by which osteoblasts could drive the inflammatory bone loss associated with staphylococcal osteomyelitis.

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