Transtriptome analysis of bone marrow-derived neutrophils after ferritin injection
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE179679 | GEO | 2021/07/09
REPOSITORIES: GEO
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Project description:Transtriptome analysis of bone marrow-derived neutrophils after ferritin injection
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Project description:Sepsis-associated acute kidney injury (SA-AKI) is a key contributor to the life threatening sequalae attributed to sepsis. Mechanistically, SA-AKI is a consequence of unabated myeloid cell activation and oxidative stress that induces tubular injury. Iron mediates inflammatory pathways directly and through regulating the expression of myeloid-derived ferritin, an iron storage protein comprised of ferritin light (FtL) and ferritin heavy chain (FtH) subunits. Previous work revealed myeloid FtH deletion leads to a compensatory increase in intracellular and circulating FtL and is associated with amelioration of SA-AKI. We designed this study to test the hypothesis that loss of myeloid FtL and subsequently, circulating FtL will exacerbate the sepsis-induced inflammatory response and worsen SA-AKI. We generated a novel myeloid-specific FtL knockout mouse (FtLLysM-/-) and induced sepsis via cecal ligation and puncture or lipopolysaccharide endotoxemia. As expected, serum ferritin levels were significantly lower in the knockout mice, suggesting that myeloid cells dominantly contribute to circulating ferritin. Interestingly, while sepsis induction led to a marked production of pro- and anti-inflammatory cytokines, there was no statistical difference between the genotypes. There was a similar loss of kidney function, as evident by a rise in serum creatinine and cystatin C, and renal injury identified by expression of kidney injury molecule-1 and neutrophil gelatinase associated lipocalin. Finally, RNA sequencing revealed upregulation of pathways for cell cycle arrest and autophagy post-sepsis, but no significant differences were observed between genotypes, including in key genes associated with ferroptosis, an iron-mediated form of cell death. The loss of FtL did not impact sepsis-mediated activation of NFkB or HIF-1a signaling, key inflammatory pathways associated with dysregulated host response. Taken together, while FtL overexpression was shown to be protective against sepsis, loss of FtL did not influence sepsis pathogenesis.
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Project description:To investigate the functional significance of myocardial ferritin heavy chain (FtH) in a model of acute myocardial infarction (MI). FtH was deleted using FtH floxed mice and Sm-22 Cre mice on a C57/bl6 background At 3 hours following 45 minutes of ischemia induced via ligation of left ant. decsending coronary artery, ischemic regions were identified, dissected, and total RNA was isolated fand gene expression profiling analysis using data obtained from RNA-seq of 3 different animals. RNA Total RNA isolated from left ventricle under homeostatic (bseline conditions) served as negative ctr. (n=3/group)
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Project description:Iron sequestration by host iron-binding proteins is an important mechanism of resistance to microbial infections. Inside oral epithelial cells, iron is stored within the ferritin, and is therefore usually not accessible to pathogenic microbes. We observed that the ferritin concentration within oral epithelial cells was directly related to their susceptibility to damage by the human pathogenic fungus Candida albicans. Thus, we hypothesized that host ferritin may be used as an iron source by this organism. A screen of C. albicans mutants lacking components of each of the three iron acquisition systems revealed that only the reductive pathway is involved in iron utilization from ferritin by this organism. Transcriptional profiling of wild-type and hyphal-defective C. albicans strains suggested that the C. albicans invasin-like protein Als3 plays a role in ferritin binding.
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Project description:Iron is an essential nutrient for humans as well as for pathogens. Hence, its correct distribution at the systemic and cellular level is mandatory for mounting an effective innate immune defense. Here we delved into the role of macrophage-expressed iron storing protein ferritin H (FTH) in immune response against the model intracellular pathogen Salmonella Typhimurium. Mice lacking FTH in the myeloid lineage (LysM-Cre+/+ Fthfl/fl) displayed impaired iron storage capacities in tissue leukocyte compartment, increased levels of labile iron in macrophages and an accelerated macrophage-mediated iron turnover. Without iron supplementation, wildtype (WT) and LysM-Cre+/+ Fthfl/fl animals showed comparable susceptibility to Salmonella infection. Interestingly, iron supplementation rapidly elicited symptoms of cytokine storm and drastically shortened survival of LysM-Cre+/+ Fthfl/fl mice. Mechanistically, we traced this phenotype back to labile iron-mediated hyperactivity of the inflammasome in FTH-deficient macrophages, culminating in excessive IL-1β secretion and secondary triggering of NF-kappaB-dependent inflammatory circuits. Accordingly, bacterial burden and cytokine levels in iron-loaded LysM-Cre+/+ Fthfl/fl mice could be effectively kept at bay by pharmacological inflammasome and IL-1β blockade. These findings point towards a previously unrecognized role of ferritin as an inhibitor of iron-dependent inflammasome activity in macrophages and a checkpoint of systemic innate response.
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Project description:Relatively brief bouts of exercise alter gene expression in peripheral blood mononuclear cells (PBMCs), but whether or not exercise changes gene expression in circulating neutrophils (whose numbers, like PBMCs, increase) is not known. We hypothesized that exercise would activate neutrophil genes involved in apoptosis, inflammation, and cell growth and repair, since these functions in leukocytes are known to be influenced by exercise. Blood was sampled before and immediately after 30-min of constant, heavy (about 80% peak O2 uptake) cycle-ergometer exercise in 12 healthy men (19-29 yr old) of average fitness. Neutrophils were isolated using density gradients; RNA was hybridized to Affymetrix U133+2 Genechip arrays. Using FDR<0.05 with 95% confidence a total of 526 genes were differentially expressed between before and after exercise. 316 genes had higher expression after exercise. The Jak/STAT pathway, known to inhibit apoptosis, was significantly activated (EASE score, p<0.005), but 14 genes were altered in a way likely to accelerate apoptosis as well. Similarly, both proinflammatory (e.g., IL32, TNFSF8 and CCR5) and anti-inflammatory (e.g., ANXA1) were affected. Growth and repair genes like AREG and FGF2 receptor genes (involved in angiogenesis) were also activated. Finally, a number of neutrophil genes known to be involved in pathological conditions like asthma and arthritis were altered by exercise, suggesting novel links between physical activity and disease or its prevention. In summary, brief heavy exercise leads to a previously unknown substantial and significant alteration in neutrophil gene expression. Experiment Overall Design: Twelve healthy men (19-29 yr old) participated in this study. A baseline blood sample was taken before the onset of exercise and immediately after 30-min exercise bout. Neutrophils were isolated using OptiPrep Density Gradient Medium (SIGMA). Total RNA was extracted using TRIzol. cRNA was hybridized onto Affymetrix U133+2 arrays (total of 24 chips).
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