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Intestinal microbiome and metabolome signatures in patients with chronic granulomatous disease.
J Allergy Clin Immunol
December 2023
Laboratory of Clinical Immunology and Microbiology (LCIM), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Md; Department of Microbiology, Infectious Diseases, and Immunology, Université de Montréal, Montreal, Quebec, Canada; Center for Immunity, Inflammation and Infectious Diseases, IRCM, Montreal, Quebec, Canada; Department of Medicine, Université de Montréal, Montreal, Quebec, Canada. Electronic address:
Background: Chronic granulomatous disease (CGD) is caused by defects in any 1 of the 6 subunits forming the nicotinamide adenine dinucleotide phosphate oxidase complex 2 (NOX2), leading to severely reduced or absent phagocyte-derived reactive oxygen species production. Almost 50% of patients with CGD have inflammatory bowel disease (CGD-IBD). While conventional IBD therapies can treat CGD-IBD, their benefits must be weighed against the risk of infection.
View Article and Find Full Text PDFCommensal bacteria augment Staphylococcus aureus infection by inactivation of phagocyte-derived reactive oxygen species.
PLoS Pathog
September 2021
Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield, United Kingdom.
Staphylococcus aureus is a human commensal organism and opportunist pathogen, causing potentially fatal disease. The presence of non-pathogenic microflora or their components, at the point of infection, dramatically increases S. aureus pathogenicity, a process termed augmentation.
View Article and Find Full Text PDFHow Microbes Defend Themselves From Incoming Hydrogen Peroxide.
Front Immunol
October 2021
Department of Microbiology, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
Microbes rely upon iron as a cofactor for many enzymes in their central metabolic processes. The reactive oxygen species (ROS) superoxide and hydrogen peroxide react rapidly with iron, and inside cells they can generate both enzyme and DNA damage. ROS are formed in some bacterial habitats by abiotic processes.
View Article and Find Full Text PDFThe use of S100 proteins testing in juvenile idiopathic arthritis and autoinflammatory diseases in a pediatric clinical setting: a retrospective analysis.
Pediatr Rheumatol Online J
January 2020
Division of Rheumatology, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH, 45229, USA.
Background: Serum phagocyte-derived alarmins S100A8/9 and S100A12 are considered useful for the assessment of inflammatory diseases. Our study evaluated the use of S100 proteins in a pediatric clinical setting for estimating disease activity and supporting diagnosis.
Methods: Patients (n = 136) who had S100 proteins tested as part of clinical care were included in this study and relevant information obtained from the medical record: C-reactive protein (CRP), disease activity status (inactive: = 0 joint; active: > 0 active joint), systemic symptoms in systemic JIA (sJIA), and symptoms of flare of other autoinflammatory and fever syndromes.
Increased ILC3s associated with higher levels of IL-1β aggravates inflammatory arthritis in mice lacking phagocytic NADPH oxidase.
Eur J Immunol
November 2019
Institute of Clinical Medicine, National Cheng-Kung University Medical College, Tainan, Taiwan.
The role of redox regulation in immune-mediated arthritis has been previously described. However, the relationship between innate immune cells, including innate lymphoid cells (ILCs) and phagocyte-derived ROS, in this process remains unclear. Here, we characterize ILCs and measure the IL-1 family cytokines along with other cytokines relevant to ILC functions and development in serum-induced arthritic joints in wild type and phagocytic NADPH oxidase (NOX2)-deficient Ncf1 mice.
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