PMID- 15865608
OWN - NLM
STAT- MEDLINE
DCOM- 20050606
LR  - 20131121
IS  - 0903-4641 (Print)
IS  - 0903-4641 (Linking)
VI  - 113
IP  - 4
DP  - 2005 Apr
TI  - Intravenous immunoglobulin preparations promote apoptosis in 
      lipopolysaccharide-stimulated neutrophils via an oxygen-dependent pathway in 
      vitro.
PG  - 269-77
AB  - Since prolonged survival of activated neutrophils has an autotoxic potential, 
      neutrophil apoptosis plays an important role in the rapid resolution of 
      inflammation. Intravenous immunoglobulin (IVIG) preparations, which are 
      beneficial therapeutic agents for the treatment of autoimmune diseases and 
      systemic inflammatory diseases, have been reported to induce apoptosis of 
      lymphocytes and endothelial cells in vitro. In the present study, we investigated 
      whether IVIG may induce apoptosis of neutrophils cultured in vitro. After 
      neutrophils prestimulated with or without lipopolysaccharide (LPS) were cultured 
      in the presence or absence of IVIG, the number of apoptotic cells, intracellular 
      H2O2 and GSH were measured by a flow cytometer. IVIG induced apoptosis of 
      LPS-stimulated neutrophils dose dependently, but not in unstimulated neutrophils. 
      Although anti-Fas monoclonal antibodies (mAbs) had no effect on the IVIG-induced 
      apoptosis in the LPS-stimulated neutrophils, anti-Fc gamma receptor (Fc gammaR) 
      II- and III-blocking mAbs significantly inhibited the IVIG-induced apoptosis. 
      IVIG increased the production of intracellular H2O2, while it decreased the 
      production of GSH, in the LPS-stimulated neutrophils. Furthermore, a specific 
      NADPH oxidase inhibitor and anti-oxidants inhibited the IVIG-induced neutrophil 
      apoptosis. Therefore, these findings indicate that IVIG preparations induce 
      apoptosis of LPS-stimulated neutrophils and suggest that the IVIG-induced 
      apoptosis may be mediated by an oxygen-dependent pathway via Fc gammaRII and III.
FAU - Takeshita, Seiichiro
AU  - Takeshita S
AD  - Ibaraki University, Faculty of Education, Ibaraki, Japan. 
      takeshit@mx.ibaraki.ac.jp
FAU - Tsujimoto, Hiroshi
AU  - Tsujimoto H
FAU - Nakatani, Keigo
AU  - Nakatani K
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Denmark
TA  - APMIS
JT  - APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
JID - 8803400
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Reactive Oxygen Species)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - *Apoptosis
MH  - Cells, Cultured
MH  - Glutathione/biosynthesis
MH  - Humans
MH  - Hydrogen Peroxide/metabolism
MH  - Immunoglobulins, Intravenous/*pharmacology
MH  - Lipopolysaccharides
MH  - Lymphocyte Activation
MH  - Neutrophils/*drug effects/immunology/physiology
MH  - Reactive Oxygen Species/metabolism
EDAT- 2005/05/04 09:00
MHDA- 2005/06/07 09:00
CRDT- 2005/05/04 09:00
PHST- 2005/05/04 09:00 [pubmed]
PHST- 2005/06/07 09:00 [medline]
PHST- 2005/05/04 09:00 [entrez]
AID - APMapm_05 [pii]
AID - 10.1111/j.1600-0463.2005.apm_05.x [doi]
PST - ppublish
SO  - APMIS. 2005 Apr;113(4):269-77. doi: 10.1111/j.1600-0463.2005.apm_05.x.