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Increased intracellular oxygen radical production in neutrophils during febrile episodes of PFAPA syndrome.

Artikel i vetenskaplig tidskrift
Författare Martina Sundqvist
Per Wekell
Veronica Osla
Johan Bylund
Karin Christenson
Karin Sävman
Dirk Foell
David A Cabral
Anders Fasth
Stefan Berg
Kelly Brown
Anna Karlsson
Publicerad i Arthritis and rheumatism
Volym 65
Nummer/häfte 11
Sidor 2971–2983
ISSN 1529-0131
Publiceringsår 2013
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Sidor 2971–2983
Språk en
Länkar dx.doi.org/10.1002/art.38134
Ämneskategorier Immunbiologi, Reumatologi och inflammation, Pediatrik

Sammanfattning

Objective: Periodic Fever, Aphthous stomatitis, Pharyngitis, and cervical Adenitis (PFAPA) syndrome is an autoinflammatory disease of unknown etiology that primarily affects preschool children. PFAPA is characterized by recurrent attacks of fever and inflammatory symptoms consistent with the disease acronym. Since autoinflammatory diseases by definition are mediated by cells of the innate immune system, we aimed at evaluating functional features of neutrophils, the most abundant innate immune cell in circulation, in PFAPA syndrome. Methods: Blood neutrophils, obtained from PFAPA patients during both febrile and asymptomatic afebrile phases of disease, as well as from healthy children (afebrile controls) and children with fever and abdominal pain (febrile controls) were analysed for three key neutrophil characteristics: (i) apoptosis (measured by Annexin V/7AAD staining), (ii) production of reactive oxygen species (ROS; by luminol/isoluminol-amplified chemiluminescence), and (iii) priming status (as responsiveness to galectin-3 and upregulation of CD11b). Results: Compared to neutrophils from both PFAPA patients in an afebrile interval and from febrile controls, neutrophils obtained during a PFAPA flare produced elevated levels of intracellular NADPH-oxidase-derived ROS, had significantly diminished rates of spontaneous apoptosis, and displayed signatures of priming. In contrast, neutrophils from afebrile PFAPA patients had a significantly elevated rate of spontaneous apoptosis compared to neutrophils from afebrile controls. Conclusions: We demonstrate that three key aspects of neutrophil innate immune function, namely apoptosis, priming, and generation of an intracellular oxidative burst are altered, most prominently during febrile attacks in PFAPA syndrome. © 2013 American College of Rheumatology.

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