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RESEARCH - A mechanistic approach to understanding CLA's role in inflammation

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Am J Physiol Regul Integr Comp Physiol 293: R669-R676, 2007. First

published June 6, 2007; doi:10.1152/ajpregu.00005.2007

INFLAMMATION AND CYTOKINES

A mechanistic approach to understanding conjugated linoleic acid's

role in inflammation using murine models of rheumatoid arthritis

E. Butz,1 Guangming Li,2 Shane M. Huebner,1 and Mark E. Cook1,2,3

1Nutritional Sciences, 2Molecular and Environmental Toxicology, and

3Animal Sciences, University of Wisconsin-Madison, Madison, Wisconsin

A naturally occurring fatty acid, conjugated linoleic acid (CLA),

reduces immune-induced TNF and inducible cyclooxygenase (COX-2)

expression; key mediators of inflammation in rheumatoid arthritis

(RA). On the basis of previous work, it was hypothesized that dietary

CLA would act as an anti-inflammatory agent in select animal models of

RA. In the collagen antibody-induced arthritis (CAIA) model, mice fed

CLA (mixed isomers of c9, t11, and t10, c12-CLA) for 3 wk before

anticollagen antibody injection had reduced lipopolysaccharide-induced

plasma TNF levels and had arthritic scores that were 60% of mice fed

corn oil (CO). In the collagen-induced arthritis (CIA) model, mice fed

mixed isomers of CLA for 21 days before immunization had lower IgG1

titers, earlier signs of joint inflammation, but similar arthritis

scores compared with CO fed mice during the remaining 70-day

post-injection period. Beginning on day 80 to 133, CLA-fed mice had

arthritic scores 70% that of the CO-fed mice. In a second CIA

experiment, CLA was fed only after the booster injection. Plasma IgG1

levels were not reduced and arthritis onset was delayed 4 days in

CLA-fed mice compared with the CO-fed mice. Peak arthritis score was

similar between CLA and CO-fed mice from day 35 to 56. Because CLA

reduced inflammation in the CAIA model, delayed onset of arthritis in

the CIA model (CIA experiment 2) and reduced arthritis score after day

80 in the CIA model (CIA experiment 1), we concluded that dietary CLA

exhibited anti-inflammatory activity that was dependent on antibody.

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Read the entire article here:

http://ajpregu.physiology.org/cgi/content/full/293/2/R669

Not an MD

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