{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Monteith AJ"],"funding":["HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","NIDDK NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","HHS | NIH | National Institute of Allergy and Infectious Diseases","Lupus Research Alliance","NCI NIH HHS","Edward P. Evans Foundation","Incyte Pharmaceuticals"],"pagination":["454-463"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8761356"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["208(2)"],"pubmed_abstract":["Inflammation involves a delicate balance between pathogen clearance and limiting host tissue damage, and perturbations in this equilibrium promote disease. Patients suffering from autoimmune diseases, such as systemic lupus erythematosus (SLE), have higher levels of serum S100A9 protein and increased risk for infection. S100A9 is highly abundant within neutrophils and modulates antimicrobial activity in response to bacterial pathogens. We reasoned that increased serum S100A9 in SLE patients reflects accumulation of S100A9 protein in neutrophils and may indicate altered neutrophil function. In this study, we demonstrate elevated S100A9 protein within neutrophils from SLE patients, and MRL/<i>lpr</i> mice associates with lower mitochondrial superoxide, decreased suicidal neutrophil extracell"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["Altered Mitochondrial Homeostasis during Systemic Lupus Erythematosus Impairs Neutrophil Extracellular Trap Formation Rendering Neutrophils Ineffective at Combating <i>Staphylococcus aureus</i>."],"pmcid":["PMC8761356"],"funding_grant_id":["R01 AI153167","R01 AI073843","R01 AI069233","P30 DK058404","F32HL144081","R01DK105550","R01AI153167","R01 DK105550","T32 DK101003","T32 AI112541","R01 AI138581","R01AI069233","P30 CA068485","R01 AI150701","R01AI073843","T32DK101003","F32 HL144081","R01 AI145992","R01AI101171","R01 AI101171"],"pubmed_authors":["Crofford LJ","Voss K","Miller JM","Rathmell JC","Williams JM","Skaar EP","Monteith AJ"],"additional_accession":[]},"is_claimable":false,"name":"Altered Mitochondrial Homeostasis during Systemic Lupus Erythematosus Impairs Neutrophil Extracellular Trap Formation Rendering Neutrophils Ineffective at Combating <i>Staphylococcus aureus</i>.","description":"Inflammation involves a delicate balance between pathogen clearance and limiting host tissue damage, and perturbations in this equilibrium promote disease. Patients suffering from autoimmune diseases, such as systemic lupus erythematosus (SLE), have higher levels of serum S100A9 protein and increased risk for infection. S100A9 is highly abundant within neutrophils and modulates antimicrobial activity in response to bacterial pathogens. We reasoned that increased serum S100A9 in SLE patients reflects accumulation of S100A9 protein in neutrophils and may indicate altered neutrophil function. In this study, we demonstrate elevated S100A9 protein within neutrophils from SLE patients, and MRL/<i>lpr</i> mice associates with lower mitochondrial superoxide, decreased suicidal neutrophil extracell","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2025-04-04T20:32:58.492Z","creation":"2025-04-04T20:32:58.492Z"},"accession":"S-EPMC8761356","cross_references":{"pubmed":["34930781"],"doi":["10.4049/jimmunol.2100752"]}}