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Prevention of bone marrow cell apoptosis and regulation of hematopoiesis by type I IFNs during systemic responses to pneumocystis (PC) lung infection

ABSTRACT: IFrag-/- but not RAG-/- mice develop rapidly progressing bone marrow failure in response to PC lung infection. Changes contributing to accelerated bone marrow cell apoptosis in IFrag-/- mice appear to be initiated around day 7 post infection. To gain further insight into the mechanism underlying the induction of bone marrow failure in IFRag-/- but not RAG-/- mice in response to PC lung infection, IFRag and RAG mice were PC infected via intra-tracheal inocculation of 10e7 nuclei and bone marrow responses were assessed at day 0, and 7 post infection. One group of IFRag-/- mice also received anti-oxidants treatment with N-Acetyl cysteine in drinking water (100mg/ml) throughout the course of infection (IFRag-/- +NAC) as oxidative stress appeared to be a contributing factor.

ORGANISM(S): Mus musculus

PROVIDER: GSE27835 | GEO | 2012/02/20

SECONDARY ACCESSION(S): PRJNA138027

REPOSITORIES: GEO

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Prevention of bone marrow cell apoptosis and regulation of hematopoiesis by type I IFNs during systemic responses to pneumocystis (PC) lung infection

Project description:IFrag-/- but not RAG-/- mice develop rapidly progressing bone marrow failure in response to PC lung infection. Changes contributing to accelerated bone marrow cell apoptosis in IFrag-/- mice appear to be initiated around day 7 post infection. To gain further insight into the mechanism underlying the induction of bone marrow failure in IFRag-/- but not RAG-/- mice in response to PC lung infection, IFRag and RAG mice were PC infected via intra-tracheal inocculation of 10e7 nuclei and bone marrow responses were assessed at day 0, and 7 post infection. One group of IFRag-/- mice also received anti-oxidants treatment with N-Acetyl cysteine in drinking water (100mg/ml) throughout the course of infection (IFRag-/- +NAC) as oxidative stress appeared to be a contributing factor. RT2 profiler PCR array, 5 conditions, 3 biological replicates

2012-02-20 | E-GEOD-27835 | biostudies-arrayexpress

ABIN1 (Q478) is required to prevent hematopoietic deficiencies through regulating type I IFNs expression

Project description:A20-binding inhibitor of NF-κB activation (ABIN1) is a polyubiquitin-binding protein that regulates cell death and immune responses. Although Abin1 (Tnip1) is located on chromosome 5q in the region commonly deleted in patients with 5q minus syndrome, the most distinct of the myelodysplastic syndromes (MDSs), the precise role of ABIN1 in MDSs remains unknown. In this study, we generated mice with a mutation that disrupts the polyubiquitin-binding site (Abin1Q478H/Q478H). These mice developed MDS-like diseases characterized by anemia, thrombocytopenia, and megakaryocyte dysplasia. Extramedullary hematopoiesis and bone marrow failure are also observed in Abin1Q478H/Q478H mice. t Notably, higher levels of type I interferon (IFN-I) expression were observed in the bone marrow cells of Abin1Q478H/Q478H mice than in those of wild-type mice. Consistently, blocking type I IFN signaling through the co-deletion of Ifnar1 greatly ameliorated anemia, thrombocytopenia, and splenomegaly in Abin1Q478H/Q478H mice. Taken together, these results demonstrated that ABIN1 (Q478) prevents the development of hematopoietic deficiencies by regulating type I IFN expression.

2023-10-15 | GSE245029 | GEO

Inherited Bone Marrow Failure Syndromes

Project description:Inherited Bone Marrow Failure Syndromes

| PRJNA417130 | ENA

Inherited Bone Marrow Failure Syndromes

Project description:Inherited Bone Marrow Failure Syndromes

| PRJNA417131 | ENA

Comparison of gene expression profile in RAG2+ B lineage cells from the small intestinal lamina propria and RAG2+ B lineage cells from the bone marrow

2013-07-12 | GSE48805 | GEO

ABIN1 mutant (Q478H) contribute to progressive myelodysplastic syndromes liked diseases by type I IFNs signaling

Project description:To understand the mechanism of MDS in Abin1Q478H/Q478H mice, we performed RNA-seq analysis of bone marrow lineage-negative cells from 5 months Abin1Q478H/Q478H mice and WT control mice to gain a global view of the transcriptome profile regulated by ABIN1(Q478H) mutation.

2023-01-08 | GSE220301 | GEO

Comparison of gene expression profile in RAG2+ B lineage cells from the small intestinal lamina propria and RAG2+ B lineage cells from the bone marrow

Project description:We used a RAG2-GFP reporter mouse to show that RAG+ B lineage cells can be found in the small intestinal lamina proria in normally-housed mice at weaning age. We used microarry expression analysis to compare the RAG2+ population in the gut to the RAG2+ B lineage population in the bone marrow. Microarray was used to compare RAG2+ lamina propria B cells to RAG2+ bone marrow B cells. For each experiment, RAG2-GFP+ cells from 8-12 post-natal day 17-25 RAG2-GFP reporter mice were sorted from small intestinal lamina propria lymphocyte preparations and bone marrow. RNA extracted from trizol was used for the analysis. 3 independent replicates were performed.

2013-07-12 | E-GEOD-48805 | biostudies-arrayexpress

Transcription profiling of human Waldenstroms macroglobulinemia CD19+ WM B cells (WM-BC) and CD138+ WM plasma cells (WM-PC) with those of normal CD19+ peripheral blood B cells (PB-BC), tonsil-BC (T-BC), CD138+ T-PC and bone marrow PC (N-PC) reveals biological insights into its pathophysiology

Project description:Waldenströms macroglobulinemia (WM) is a rare lymphoproliferative disorder with apparent morphologic and immunophenotypic heterogeneity and its origins are still poorly understood. In this study, using Gene-Expression Profiling (GEP), we compared the global mRNA expression patterns of CD19+ WM B cells (WM-BC) and CD138+ WM plasma cells (WM-PC) with those of normal CD19+ peripheral blood B cells (PB-BC), tonsil-BC (T-BC), CD138+ T-PC and bone marrow PC (N-PC). Experiment Overall Design: The sample cohort studied consisted of CD19-selected peripheral blood B cells (PB-BC; n = 7), tonsil B cells (T-BC; n = 7), bone marrow B cells from WM (WM-BC; n = 12), tonsil plasma cells (T-PC; n = 9), bone marrow plasma cells from healthy donors (N-PC; n = 10), WM plasma cells (WM-PC, n = 9), and MM plasma cells (MM-PC; n = 11).

2008-12-05 | E-GEOD-9656 | biostudies-arrayexpress

Knockdown of TERC with siRNA in normal bone marrow stromal cells (BMSCs) recapitulates the defective BMSC phenotype in patients with telomere biology disorders

Project description:Dyskeratosis congenita (DC) is an inherited multi-system disorder, characterized by oral leukoplakia, nail dystrophy, and abnormal skin pigmentation, as well as high rates of bone marrow failure, solid tumors, and other medical problems such as osteopenia. DC and telomere biology disorders (collectively referred to as TBD here) are caused by germline mutations in telomere biology genes leading to very short telomeres and limited proliferative potential of hematopoietic stem cells. We found that skeletal stem cells (SSCs) within the bone marrow stromal cell population (BMSCs, also known as bone marrow-derived mesenchymal stem cells), may contribute to the hematological phenotype. TBD-BMSCs exhibited reduced clonogenicity, reduced telomerase activity, spontaneous differentiation into adipocytes and fibrotic cells, and increased senescence in vitro. Upon in vivo transplantation into mice, TBD-BMSCs failed to form bone or support hematopoiesis, unlike normal BMSCs. TERC reduction (a TBD-associated gene) in normal BMSCs by siTERC-RNA recapitulated the TBD-BMSC phenotype by reducing proliferation and secondary colony forming efficiency, and by accelerating senescence in vitro. Microarray profiles of control and siTERC-BMSCs showed decreased hematopoietic factors at the mRNA level, and decreased secretion of factors at the protein level. These findings are consistent with defects in SSCs/BMSCs contributing to bone marrow failure in TBD.

2014-12-09 | GSE64023 | GEO

Efficacy of JAK 1/2 inhibition in murine immune bone marrow failure

Project description:Background and methods: Ruxolitinib (RUX) is a Jak inhibitor that is used in the treatment of intermediate or high risk myelofibrosis and resistant forms of polycythemia vera and graft-vs-host disease due to its efficacy of reducing inflammatory cytokines and markers of inflammation. We tested its potential therapeutic effects in murine models of immune-mediated bone marrow failure. RNA-Seq and analysis was performed using NEBNext Ultra™ II RNA Library Prep Kit for Illumina and Illumina Novaseq6000, according to the Institute's protocols. Results: As both prophylaxis and therapy, Ruxolitinib improved pancytopenia and BM cellularity and decreased BM T cell infiltration in bone marrow failure mice. RNA sequencing demonstrated that Ruxolitinib suppressed expression of inflammtory genes in bone marrow infiltrated CD8 T cells compared with untreated mice. Conclusion: Our results demonstrate that Ruxolitinib is highly effective in attenuation of disease and extending survival of immune-mediated bone marrow failure mice.

2023-01-29 | GSE196645 | GEO

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