title: Degradation of neutrophil extracellular traps is decreased in patients with antiphospholipid syndrome.
abstract: OBJECTIVE
  A decreased ability to degrade neutrophil extracellular traps (NETs) is seen in a subgroup of patients with systemic lupus erythematosus (SLE) and correlates with the presence of autoantibodies. Antiphospholipid syndrome (APS) can develop secondary to SLE or as a primary disease. In the current study we investigated the ability of sera from patients with APS to degrade NETs. The presence of antibodies against NETs and neutrophil remnants were also determined in the same patients.
  
  
  METHODS
  In the study, 106 patients with APS (73 primary and 33 secondary), 76 patients with systemic sclerosis (SSc) and 77 healthy donors as control samples were included. NETs generated from neutrophils isolated from healthy volunteers were incubated with patient sera, followed by measurement of degraded NETs or deposited IgG.
  
  
  RESULTS
  Sera of APS patients had a decreased ability to degrade NETs compared to healthy controls, with no difference between primary and secondary APS. Sera from SSc patients did not differ significantly from healthy controls in the ability to degrade NETs. A decreased degradation of NETs correlated weakly to increased levels of antibodies against NETs/neutrophil remnants in patients with primary APS, but stronger in patients with secondary APS.
  
  
  CONCLUSIONS
  The ability to degrade NETs is decreased in a subgroup of patients with APS and is associated with antibodies against NETs and specific clinical manifestations in those patients.
authors.affiliation: Lund University, Department of Laboratory Medicine, Section of Medical Protein Chemistry, Malmo, Sweden. jonatan.leffler@med.lu.se.
authors.forename: Jonatan
authors.initials: J
authors.lastname: Leffler
authors.forename: Ljudmila
authors.initials: L
authors.lastname: Stojanovich
authors.forename: Yehuda
authors.initials: Y
authors.lastname: Shoenfeld
authors.forename: Gordana
authors.initials: G
authors.lastname: Bogdanovic
authors.forename: Roger
authors.initials: R
authors.lastname: Hesselstrand
authors.forename: Anna M
authors.initials: AM
authors.lastname: Blom
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016736:Antiphospholipid Syndrome / Q000175:diagnosis / Q000276:immunology / Q000378:metabolism*; D001323:Autoantibodies / Q000097:blood; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D002843:Chromatin / Q000276:immunology / Q000378:metabolism*; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism*; D012595:Scleroderma, Systemic / Q000097:blood / Q000276:immunology; D055815:Young Adult; D023084:alpha-Defensins / Q000276:immunology / Q000378:metabolism*
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D002843:Chromatin; D007074:Immunoglobulin G; D023084:alpha-Defensins