Mechanisms of increased survival after lipopolysaccharide-induced endotoxic shock in mice consuming olive oil-enriched diet

• Published in: Shock (Augusta, Ga.) Ga.), 2005-02, Vol.23 (2), p.173-178
• Main Authors: LEITE, Milane S, PACHECO, Patricia, GOMES, Rachel N, GUEDES, Alexandre T, CASTRO-FARIA, Hugo C, BOZZA, Patricia T, KOATZ, Vera Lucia G
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animal Feed; Animals; Biological and medical sciences; Blood coagulation. Blood cells; Body Weight; Canola Oil; Cell Movement; Cell Survival; Chemokine CCL2 - metabolism; Cytokines - metabolism; Diet; Dinoprostone - metabolism; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care; Endotoxins - metabolism; Escherichia coli - metabolism; Fatty Acids - metabolism; Fatty Acids, Monounsaturated; Female; Fundamental and applied biological sciences. Psychology; Inflammation; Intensive care medicine; Interleukin-10 - metabolism; Interleukin-6 - metabolism; Leukotriene B4 - metabolism; Lipopolysaccharides - metabolism; Medical sciences; Mice; Mice, Inbred C57BL; Molecular and cellular biology; Neutrophils - metabolism; Olive Oil; Plant Oils - metabolism; Platelet; Sesame Oil; Shock, Septic - metabolism; Soybean Oil; Time Factors; Tumor Necrosis Factor-alpha - metabolism
• ISSN: 1073-2322
• DOI: 10.1097/01.shk.0000148072.12094.77

We examined the impact of dietary fatty acid intake on lipopolysaccharide (LPS)-induced endotoxic shock. C57Bl/6J mice were fed for 6 weeks with a commercial laboratory chow (CC) or with test chows containing 7% (w/w) canola oil (CO), sesame oil (SeO), soybean oil (SO), or virgin olive oil (OO). The increase in body weight and energy consumption were similar for all diets tested. In the sixth week, mice were injected intraperitoneally with 400 microg of bacterial LPS to induce endotoxic shock. LPS induced a massive neutrophil infiltration into the peritoneal cavity and an increase in lipid body (LB) formation in leukocytes recovered from the peritoneal fluid of mice fed with CC, CO, SeO, or SO. In addition, there were increases in prostaglandin E(2) (PGE(2)), leukotriene B4 (LTB(4)), and cytokines IL-6, IL-10, and MCP-1 in peritoneal lavage, as well as in plasma TNF-alpha. In contrast, mice fed with OO exhibited reduced neutrophil accumulation and LB formation, and also had lower levels of PGE(2), LTB(4), MCP-1, and TNF-alpha. All mice fed with CC, CO, SeO, or SO died within 48 to 72 h after LPS injection. Interestingly, mice fed with the OO diet were resistant to endotoxic shock, with 60% survival at 168 h. These data indicate that intake of OO may have a beneficial role, reducing the magnitude of the inflammatory process triggered by endotoxic shock through modulation of LB formation and of the production of inflammatory mediators.