PMID- 21420242
OWN - NLM
STAT- MEDLINE
DCOM- 20110915
LR  - 20110513
IS  - 1532-2777 (Electronic)
IS  - 0306-9877 (Linking)
VI  - 76
IP  - 6
DP  - 2011 Jun
TI  - Short chain fatty acids may elicit an innate immune response from preadipocytes: 
      a potential link between bacterial infection and inflammatory diseases.
PG  - 881-3
LID - 10.1016/j.mehy.2011.02.041 [doi]
AB  - Short chain fatty acids (SCFAs) such as acetate, propionate and butyrate are 
      produced by bacterial fermentation of dietary fiber. The highest concentrations 
      of SCFAs in the body are found in the colon. Elevated dietary acetate has been 
      shown to have anti-inflammatory effects in mouse models of colitis and 
      inflammatory diseases in peripheral tissues. The details of how dietary SCFAs 
      stimulate reduced inflammation in peripheral tissues have not been determined. I 
      suggest that SCFA concentrations in peripheral tissues are generally not 
      sufficient to locally produce a significant anti-inflammatory effect from immune 
      cells. Moreover it is possible that elevated SCFA levels in peripheral tissues 
      may actually stimulate an inflammatory response. The hypothesis is presented that 
      preadipocytes and other cells with immune function such as fibroblasts in 
      peripheral tissues elicit an inflammatory innate immune response when exposed to 
      SCFAs at millimolar concentrations. A role for SCFAs in activating an immune 
      response in preadipocytes is possible given the expression of a SCFA receptor in 
      these cells, the demonstration that adipocytes and preadipocytes have immunity 
      related functions, the observation that 2mM SCFAs stimulated the expression of 
      monocyte chemoattractant protein-1 (MCP-1) mRNA from 3T3-L1 preadipocytes and 
      that concentrations of SCFAs can reach elevated levels at sites of bacterial 
      infection. A SCFA-induced inflammatory response from preadipocytes and other 
      cells with immune function, such as fibroblasts, may provide a further 
      contributing factor linking bacterial infection to the development of insulin 
      resistance and the severity of inflammatory diseases such as atherosclerosis.
CI  - Copyright (c) 2011 Elsevier Ltd. All rights reserved.
FAU - Garland, S H
AU  - Garland SH
AD  - School of Public Health, Tropical Medicine and Rehabilitation Science, James Cook 
      University, Qld 4811, Australia. Stephen.Garland@jcu.edu.au
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110321
PL  - United States
TA  - Med Hypotheses
JT  - Medical hypotheses
JID - 7505668
RN  - 0 (Fatty Acids)
SB  - IM
MH  - Adipocytes/*drug effects/immunology
MH  - Bacterial Infections/complications/*immunology
MH  - Fatty Acids/*pharmacology
MH  - Humans
MH  - Immunity, Innate/*drug effects
MH  - Inflammation/complications/*immunology
EDAT- 2011/03/23 06:00
MHDA- 2011/09/16 06:00
CRDT- 2011/03/23 06:00
PHST- 2010/11/26 00:00 [received]
PHST- 2011/02/24 00:00 [accepted]
PHST- 2011/03/23 06:00 [entrez]
PHST- 2011/03/23 06:00 [pubmed]
PHST- 2011/09/16 06:00 [medline]
AID - S0306-9877(11)00099-5 [pii]
AID - 10.1016/j.mehy.2011.02.041 [doi]
PST - ppublish
SO  - Med Hypotheses. 2011 Jun;76(6):881-3. doi: 10.1016/j.mehy.2011.02.041. Epub 2011 
      Mar 21.