title: Omega-3 fatty acid intervention suppresses lipopolysaccharide-induced inflammation and weight loss in mice.
abstract: Bacterial endotoxin lipopolysaccharide (LPS)-induced sepsis is a critical medical condition, characterized by a severe systemic inflammation and rapid loss of muscle mass. Preventive and therapeutic strategies for this complex disease are still lacking. Here, we evaluated the effect of omega-3 (n-3) polyunsaturated fatty acid (PUFA) intervention on LPS-challenged mice with respect to inflammation, body weight and the expression of Toll-like receptor 4 (TLR4) pathway components. LPS administration induced a dramatic loss of body weight within two days. Treatment with n-3 PUFA not only stopped loss of body weight but also gradually reversed it back to baseline levels within one week. Accordingly, the animals treated with n-3 PUFA exhibited markedly lower levels of inflammatory cytokines or markers in plasma and tissues, as well as down-regulation of TLR4 pathway components compared to animals without n-3 PUFA treatment or those treated with omega-6 PUFA. Our data demonstrate that n-3 PUFA intervention can suppress LPS-induced inflammation and weight loss via, at least in part, down-regulation of pro-inflammatory targets of the TLR4 signaling pathway, and highlight the therapeutic potential of n-3 PUFA in the management of sepsis.
authors.affiliation: Laboratory for Lipid Medicine and Technology (LLMT), Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA. liuyinghua77@hotmail.com.|Nutrition Department, People's Liberation Army General Hospital, Beijing 100853, China. liuyinghua77@hotmail.com.
authors.forename: Ying-Hua
authors.initials: YH
authors.lastname: Liu
authors.affiliation: Laboratory for Lipid Medicine and Technology (LLMT), Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA. xyli75@126.com.|Institute of Biochemistry and Molecular Biology, Guangdong Medical College, Zhanjiang, Guangdong 524023, China. xyli75@126.com.
authors.forename: Xiang-Yong
authors.initials: XY
authors.lastname: Li
authors.affiliation: Laboratory for Lipid Medicine and Technology (LLMT), Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA. cchen45@mgh.harvard.edu.
authors.forename: Chih-Yu
authors.initials: CY
authors.lastname: Chen
authors.affiliation: Laboratory for Lipid Medicine and Technology (LLMT), Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA. hmzhang9607@sina.com.
authors.forename: Hong-Man
authors.initials: HM
authors.lastname: Zhang
authors.affiliation: Laboratory for Lipid Medicine and Technology (LLMT), Massachusetts General Hospital and Harvard Medical School, Boston, MA 02129, USA. kang.jing@mgh.harvard.edu.
authors.forename: Jing X
authors.initials: JX
authors.lastname: Kang
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D016207:Cytokines / Q000097:blood; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D007249:Inflammation / Q000139:chemically induced / Q000517:prevention & control*; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors* / Q000633:toxicity; D051379:Mice; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis; D015431:Weight Loss / Q000187:drug effects*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D015525:Fatty Acids, Omega-3; D008070:Lipopolysaccharides; C493487:Tlr4 protein, mouse; D051197:Toll-Like Receptor 4