PMID- 11689209
OWN - NLM
STAT- MEDLINE
DCOM- 20020204
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 159
IP  - 1
DP  - 2001 Nov
TI  - The effect of intravenous immunoglobulins on intimal thickening in a mouse model 
      of arterial injury.
PG  - 77-83
AB  - Inflammatory mechanisms appear to influence the progression of intimal thickening 
      in experimental models of arterial injury. Intravenous immunoglobulin (IVIG) is a 
      polyspecific preparation of human immunoglobulin (Ig)G employed for treatment of 
      autoimmune disorders. In this study, we sought to investigate whether treatment 
      with IVIG could influence intimal thickening in a model of murine arterial 
      injury. Intimal thickening was induced by placement of a periadventitial cuff 
      over the right femoral artery of male C57BL/6 mice. In the first experiment, IVIG 
      or human serum albumin (HSA) (10 mg/mouse) were administered intraperitoneally 
      for five consecutive days starting 1 day prior to cuff placement. In the second 
      experiment, IVIG or HSA treatment were delivered similarly, but initiated 3 days 
      following induction of arterial injury. Neointimal area and intimal/medial ratio 
      were significantly reduced in mice treated with IVIG prior to cuff placement as 
      compared with HSA treatment. No differences were noted with regard to neointimal 
      area or intimal/medial ratio, between IVIG- and HSA-treated mice when the 
      treatment was commenced 3 days following induction of injury. IVIG treatment 
      reduced the proliferative capacity of splenocytes to the non-specific mitogen 
      Con-A. Treatment with IVIG was associated with a significantly enhanced secretion 
      of interleukin (IL)-10) by the respective splenocytes in comparison with 
      HSA-treated mice. No effect of IVIG was evident on the secretion of IL-4 or 
      IFN-gamma. Thus, IVIG has proven beneficial in ameliorating intimal thickening in 
      a mouse model of arterial injury. The effect could be mediated by upregulation of 
      T-cell secretion of the anti-inflammatory cytokine IL-10.
FAU - Keren, G
AU  - Keren G
AD  - Department of Cardiology and the Cardiovascular Research Laboratory, Ichilov 
      Hospital, Elias Sourasky Tel-Aviv Medical Center, 6 Weizman Street, Tel-Aviv, 
      Israel. kereng@tasmc.health.gov.il
FAU - Keren, P
AU  - Keren P
FAU - Barshack, I
AU  - Barshack I
FAU - Pri-Chen, S
AU  - Pri-Chen S
FAU - George, J
AU  - George J
LA  - eng
PT  - Journal Article
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Immunoglobulins, Intravenous)
RN  - 0 (Serum Albumin)
RN  - 130068-27-8 (Interleukin-10)
RN  - 207137-56-2 (Interleukin-4)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Femoral Artery/*injuries/*pathology
MH  - Immunoglobulins, Intravenous/*pharmacology
MH  - Interferon-gamma/biosynthesis
MH  - Interleukin-10/biosynthesis
MH  - Interleukin-4/biosynthesis
MH  - Lymphocyte Activation/drug effects
MH  - Lymphocytes/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Serum Albumin/pharmacology
MH  - Tunica Intima/drug effects/*pathology
EDAT- 2001/11/02 10:00
MHDA- 2002/02/05 10:01
CRDT- 2001/11/02 10:00
PHST- 2001/11/02 10:00 [pubmed]
PHST- 2002/02/05 10:01 [medline]
PHST- 2001/11/02 10:00 [entrez]
AID - S0021-9150(01)00491-9 [pii]
AID - 10.1016/s0021-9150(01)00491-9 [doi]
PST - ppublish
SO  - Atherosclerosis. 2001 Nov;159(1):77-83. doi: 10.1016/s0021-9150(01)00491-9.