R3230AC rat mammary tumor and dietary long-chain (n-3) fatty acids change immune cell composition and function during mitogen activation

Citation
Le. Robinson et al., R3230AC rat mammary tumor and dietary long-chain (n-3) fatty acids change immune cell composition and function during mitogen activation, J NUTR, 131(7), 2001, pp. 2021-2027
Citations number
38
Categorie Soggetti
Food Science/Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF NUTRITION
ISSN journal
00223166 → ACNP
Volume
131
Issue
7
Year of publication
2001
Pages
2021 - 2027
Database
ISI
SICI code
0022-3166(200107)131:7<2021:RRMTAD>2.0.ZU;2-H
Abstract
Because anticancer immunity declines progressively with tumor growth, a maj or focus of current research in tumor immunology is the development of mean s to stimulate the host immune system. This study determined the effects of dietary long-chain (n-3) fatty acids and tumor burden on immune cell phosp holipid composition and membrane-mediated immune defense in rats implanted with the R3230AC mammary adenocarcinoma. Fischer 344 rats (145 +/- 2 g) wer e fed one of two semipurified diets (20 g/100 g fat) for 21 d before and 17 d after tumor implantation, Diets provided long-chain (n-3) fatty acids at 0 or 50 g/kg of total fat. Mammary tumor growth was 31% lower (P = 0.1) in rats fed long-chain (n-3) fatty acids. Dietary long-chain (n-3) fatty acid s had beneficial effects on several host immune defenses, including activat ion of CD8(+) T cells and type-1 cytokine (interferon-gamma and tumor necro sis factor-alpha) production (P < 0.05). Upregulated immune function in tum or-bearing rats fed the high (n-3) diet occurred concurrently with specific changes in the major membrane phospholipids phosphatidylcholine and phosph atidylethanolamine in high (n-3)-fed rats. Because membrane composition pla ys a critical role in immune function, additional work is needed to determi ne the relationship between alterations in the phospholipid composition of immune cells during cancer and subsequent upregulation of host defense in t he tumor-bearing state.