Mechanisms of increased survival after lipopolysaccharide-induced endotoxic shock in mice consuming olive oil-enriched diet.
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.
Leite
Milane S
MS
Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21941-590, Brazil.
Pacheco
Patrícia
P
Gomes
Rachel N
RN
Guedes
Alexandre T
AT
Castro-Faria-Neto
Hugo C
HC
Bozza
Patrícia T
PT
Koatz
Vera Lúcia G
VL
D000821:Animal Feed; D000818:Animals; D001835:Body Weight; D002465:Cell Movement; D002470:Cell Survival; D018932:Chemokine CCL2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004032:Diet; D015232:Dinoprostone / Q000378:metabolism; D004731:Endotoxins / Q000378:metabolism; D004926:Escherichia coli / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism; D005229:Fatty Acids, Monounsaturated; D005260:Female; D007249:Inflammation; D016753:Interleukin-10 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007975:Leukotriene B4 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D009504:Neutrophils / Q000378:metabolism; D000069463:Olive Oil; D010938:Plant Oils / Q000378:metabolism*; D000074262:Rapeseed Oil; D012715:Sesame Oil; D012772:Shock, Septic / Q000378:metabolism*; D013024:Soybean Oil; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D018932:Chemokine CCL2; D016207:Cytokines; D004731:Endotoxins; D005227:Fatty Acids; D005229:Fatty Acids, Monounsaturated; D015850:Interleukin-6; D008070:Lipopolysaccharides; D000069463:Olive Oil; D010938:Plant Oils; D000074262:Rapeseed Oil; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007975:Leukotriene B4; D013024:Soybean Oil; D012715:Sesame Oil; D015232:Dinoprostone