PMID- 18782326
OWN - NLM
STAT- MEDLINE
DCOM- 20081204
LR  - 20211020
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 154
IP  - 2
DP  - 2008 Nov
TI  - High mortality rate of (NZW x BXSB)F1 mice induced by administration of 
      lipopolysaccharide attributes to high production of tumour necrosis factor-alpha 
      by increased numbers of dendritic cells.
PG  - 285-93
LID - 10.1111/j.1365-2249.2008.03759.x [doi]
AB  - (NZW x BXSB)F1 mice (W/BF1 mice) have been reported to be a type of 
      autoimmune-prone mice, showing symptoms of proteinuria, anti-DNA antibodies and 
      anti-platelet antibodies. In this paper, we report that W/BF1 mice show 
      hyperproduction of tumour necrosis factor (TNF)-alpha, responding to 
      lipopolysaccharide (LPS) in comparison with normal mice, resulting in induction 
      of death. In normal mice, monocytes/macrophages (Mo/MO) are the main producer of 
      TNF-alpha, while both Mo/MO and dendritic cells (DCs) produce TNF-alpha in W/BF1 
      mice. Because the number of DCs is higher in W/BF1 mice, the main producers of 
      TNF-alpha in W/BF1 mice are thought to be DCs. Moreover, administration of 
      anti-TNF-alpha antibodies rescued the W/BF1 mice from death induced by LPS, 
      suggesting that TNF-alpha is crucial for the effect of LPS. Although there is no 
      significant difference in the expression of Toll-like receptor-4 (TLR-4) on DCs 
      between B6 and W/BF1 mice, nuclear factor kappa b activity of DCs from W/BF1 mice 
      is augmented under stimulation of LPS in comparison with that of normal mice. 
      These results suggest that the signal transduction from TLR-4 is augmented in 
      W/BF1 mice in comparison with normal mice, resulting in the hyperproduction of 
      TNF-alpha and reduced survival rate. The results also suggest that not only the 
      quantity of endotoxin, but also the host conditions, the facility to translate 
      signal from TLR, and so on, could reflect the degree of bacterial infections and 
      prognosis.
FAU - Koike-Kiriyama, N
AU  - Koike-Kiriyama N
AD  - First Department of Pathology, Kansai Medical University, Moriguchi City, Osaka, 
      Japan.
FAU - Adachi, Y
AU  - Adachi Y
FAU - Iwasaki, M
AU  - Iwasaki M
FAU - Amou, Y
AU  - Amou Y
FAU - Shigematsu, A
AU  - Shigematsu A
FAU - Koike, Y
AU  - Koike Y
FAU - Minamino, K
AU  - Minamino K
FAU - Mukaide, H
AU  - Mukaide H
FAU - Shi, M
AU  - Shi M
FAU - Yanai, S
AU  - Yanai S
FAU - Matsumura, M
AU  - Matsumura M
FAU - Ikehara, S
AU  - Ikehara S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080908
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Tlr4 protein, mouse)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Autoimmune Diseases/*immunology
MH  - Dendritic Cells/*immunology
MH  - Dose-Response Relationship, Immunologic
MH  - Female
MH  - Lipopolysaccharides/immunology/*toxicity
MH  - Male
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Signal Transduction/immunology
MH  - Spleen/immunology
MH  - Survival Analysis
MH  - Toll-Like Receptor 4/metabolism
MH  - Tumor Necrosis Factor-alpha/*biosynthesis/immunology
PMC - PMC2612720
EDAT- 2008/09/11 09:00
MHDA- 2008/12/17 09:00
PMCR- 2009/11/01
CRDT- 2008/09/11 09:00
PHST- 2008/09/11 09:00 [pubmed]
PHST- 2008/12/17 09:00 [medline]
PHST- 2008/09/11 09:00 [entrez]
PHST- 2009/11/01 00:00 [pmc-release]
AID - CEI3759 [pii]
AID - 10.1111/j.1365-2249.2008.03759.x [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2008 Nov;154(2):285-93. doi: 10.1111/j.1365-2249.2008.03759.x. 
      Epub 2008 Sep 8.