title: Neutrophils in multiple sclerosis are characterized by a primed phenotype.
abstract: Neutrophils are armed with proteases with indiscriminate histotoxic potential, and to minimize tissue injury, their activation involves priming with inflammatory mediators before cells are fully activated in a second step. Here, we show that neutrophils in multiple sclerosis patients are more numerous and exhibit a primed state based on reduced apoptosis, higher expression of TLR-2, fMLP receptor, IL-8 receptor and CD43, enhanced degranulation and oxidative burst as well as higher levels of neutrophil extracellular traps in serum. The chronic inflammatory environment in multiple sclerosis probably underlies this inappropriate neutrophil priming, which may result in enhanced neutrophil activation during infection.
authors.affiliation: Institute for Neuroimmunology and Clinical MS Research (inims), Center for Molecular Neurobiology Hamburg (ZMNH), University Medical Center-Eppendorf, Falkenried 94, 20251 Hamburg (UKE), Germany.
authors.forename: Matthias
authors.initials: M
authors.lastname: Naegele
authors.forename: Kati
authors.initials: K
authors.lastname: Tillack
authors.forename: Stefanie
authors.initials: S
authors.lastname: Reinhardt
authors.forename: Sven
authors.initials: S
authors.lastname: Schippling
authors.forename: Roland
authors.initials: R
authors.lastname: Martin
authors.forename: Mireia
authors.initials: M
authors.lastname: Sospedra
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D015550:Cell Degranulation / Q000276:immunology; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D020528:Multiple Sclerosis, Chronic Progressive / Q000097:blood / Q000235:genetics* / Q000276:immunology*; D020529:Multiple Sclerosis, Relapsing-Remitting / Q000097:blood / Q000235:genetics* / Q000276:immunology*; D018375:Neutrophil Activation / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D010641:Phenotype
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators