PMID- 16316421
OWN - NLM
STAT- MEDLINE
DCOM- 20060119
LR  - 20101118
IS  - 0300-9475 (Print)
IS  - 0300-9475 (Linking)
VI  - 62
IP  - 6
DP  - 2005 Dec
TI  - Neutrophil activation in anti-proteinase 3-positive vasculitis--a prospective 
      study.
PG  - 539-45
AB  - In vitro studies have demonstrated that antineutrophil cytoplasmic antibodies 
      (ANCA) have the capacity to activate neutrophils. Whether circulating neutrophils 
      in patients with vasculitis are activated is under debate. Eight consecutive 
      patients with antiproteinase 3 (PR3) positive acute vasculitis were included in 
      this prospective study. Neutrophil expression of adhesion molecules, Fc-receptors 
      and the ANCA-antigen PR3 was analysed and clinical characteristics were 
      documented at inclusion and after 1, 3, 6 and 9 months in the same individuals. 
      As additional markers of inflammation and endothelial activation interleukin-8 
      and soluble vascular cell adhesion molecule-1 in serum were analysed at the same 
      time points. The expression of adhesion molecules on circulating neutrophils, 
      CD62L and CD11b after in vitro N-formyl-methionyl-leucyl-phenylalanine 
      stimulation was significantly decreased at diagnosis and after 1 month but 
      returned to normal levels after 3-9 months. The neutrophil expression of 
      Fc-receptor IIIb (CD 16) was decreased at diagnosis but normalized after 1-9 
      months. The main finding was an activated neutrophil adhesion phenotype at 
      diagnosis and after 1 month, with normalized expression of adhesion molecules at 
      3-9 months. A pathological regulation of adhesion molecules may have implications 
      on the endothelial damage seen in vasculitis.
FAU - Wikman, A
AU  - Wikman A
AD  - Division of Clinical Immunology, and Transfusion Medicine, Karolinska University 
      Hospital and Karolinske Institute, Stockholm, Sweden. agneta.wikman@karolinska.se
FAU - Lundahl, J
AU  - Lundahl J
FAU - Jacobson, S H
AU  - Jacobson SH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Scand J Immunol
JT  - Scandinavian journal of immunology
JID - 0323767
RN  - 0 (Antibodies, Antineutrophil Cytoplasmic)
RN  - 0 (Antigens, CD)
RN  - 0 (FCGR3B protein, human)
RN  - 0 (GPI-Linked Proteins)
RN  - 0 (Interleukin-8)
RN  - 0 (Receptors, IgG)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126880-86-2 (L-Selectin)
RN  - EC 3.4.21.- (Serine Endopeptidases)
RN  - EC 3.4.21.76 (Myeloblastin)
SB  - IM
MH  - Antibodies, Antineutrophil Cytoplasmic/biosynthesis/*blood/physiology
MH  - Antigens, CD/blood
MH  - GPI-Linked Proteins
MH  - Humans
MH  - Interleukin-8/blood
MH  - L-Selectin/metabolism
MH  - Myeloblastin
MH  - *Neutrophil Activation/immunology
MH  - Neutrophils/*enzymology/*immunology/metabolism
MH  - Prospective Studies
MH  - Receptors, IgG/blood
MH  - Serine Endopeptidases/blood/*immunology
MH  - Vascular Cell Adhesion Molecule-1/metabolism
MH  - Vasculitis/blood/*enzymology/*immunology
EDAT- 2005/12/01 09:00
MHDA- 2006/01/20 09:00
CRDT- 2005/12/01 09:00
PHST- 2005/12/01 09:00 [pubmed]
PHST- 2006/01/20 09:00 [medline]
PHST- 2005/12/01 09:00 [entrez]
AID - SJI1695 [pii]
AID - 10.1111/j.1365-3083.2005.01695.x [doi]
PST - ppublish
SO  - Scand J Immunol. 2005 Dec;62(6):539-45. doi: 10.1111/j.1365-3083.2005.01695.x.