PMID- 16962071
OWN - NLM
STAT- MEDLINE
DCOM- 20061107
LR  - 20071114
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 349
IP  - 3
DP  - 2006 Oct 27
TI  - Inhibition of inflammatory response in transgenic fat-1 mice on a 
      calorie-restricted diet.
PG  - 925-30
AB  - Both n-3 fatty acids (n-3 FA) and calorie-restriction (CR) exert 
      anti-inflammatory effects in animal models of autoimmunity and inflammation. In 
      the present study we investigated the synergistic anti-inflammatory effects of 
      n-3 FA and CR on LPS-mediated inflammatory responses using fat-1 transgenic mice 
      that generate n-3 FA endogenously. Wild-type (WT) and fat-1 mice were maintained 
      on ad libitum (AL) or CR (40% less than AL) diet for 5 mo; splenocytes were 
      cultured in vitro with/without LPS. Our results show: (i) no difference in body 
      weights between WT and fat-1 mice on AL or CR diets, (ii) lower n-6/n-3 FA ratio 
      in splenocytes from fat-1 mice on both AL and CR diets, (iii) significant 
      reduction in NF-kappaB (p65/p50) and AP-1 (c-Fos/c-Jun) DNA-binding activities in 
      splenocytes from fat-1/CR mice following LPS treatment, and (iv) significant 
      reduction in kappaB- and AP-1-responsive IL-6 and TNF-alpha secretion following 
      LPS treatment in splenocytes from fat-1/CR mice. The inhibition of LPS-mediated 
      effects was more pronounced in fat-1/CR mice when compared to fat-1/AL or WT/CR 
      mice. These data show that transgenic expression of fat-1 results in decreased 
      pro-inflammatory n-6 FA, and demonstrate for the first time that splenocytes from 
      fat-1 mice on CR diet exhibit reduced pro-inflammatory response when challenged 
      with LPS. These results suggest that n-3 lipids with moderate CR may confer 
      protection in autoimmune and inflammatory diseases.
FAU - Bhattacharya, Arunabh
AU  - Bhattacharya A
AD  - Department of Medicine, Division of Clinical Immunology and Rheumatology, 
      University of Texas Health Science Center, San Antonio, TX 78229, USA.
FAU - Chandrasekar, Bysani
AU  - Chandrasekar B
FAU - Rahman, Md Mizanur
AU  - Rahman MM
FAU - Banu, Jameela
AU  - Banu J
FAU - Kang, Jing X
AU  - Kang JX
FAU - Fernandes, Gabriel
AU  - Fernandes G
LA  - eng
GR  - AG023648/AG/NIA NIH HHS/United States
GR  - AG027562/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20060824
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Cytokines)
RN  - 0 (Fatty Acids)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Transcription Factor AP-1)
SB  - IM
MH  - Animals
MH  - Body Weight
MH  - *Caloric Restriction
MH  - Cells, Cultured
MH  - Cytokines/metabolism
MH  - Fatty Acids/metabolism
MH  - Inflammation/chemically induced/diet therapy/genetics/*metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Mutant Strains
MH  - Mice, Transgenic
MH  - NF-kappa B/metabolism
MH  - Phenotype
MH  - Spleen/drug effects/metabolism
MH  - Transcription Factor AP-1/metabolism
EDAT- 2006/09/12 09:00
MHDA- 2006/11/09 09:00
CRDT- 2006/09/12 09:00
PHST- 2006/08/03 00:00 [received]
PHST- 2006/08/17 00:00 [accepted]
PHST- 2006/09/12 09:00 [pubmed]
PHST- 2006/11/09 09:00 [medline]
PHST- 2006/09/12 09:00 [entrez]
AID - S0006-291X(06)01913-9 [pii]
AID - 10.1016/j.bbrc.2006.08.093 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2006 Oct 27;349(3):925-30. doi: 
      10.1016/j.bbrc.2006.08.093. Epub 2006 Aug 24.