Increased survival after a cecal ligation and puncture-induced sepsis in mice consuming oleic acid

Introduction

Sepsis accounts for a huge number of deaths in ICUs worldwide. Sepsis describes a complex clinical syndrome that results from an infection, setting off a cascade of systemic inflammatory responses that can lead to multiple organ failure and death. Leite and colleagues have shown that mice fed for 6 weeks with an olive oil diet were resistant to endotoxic shock, with 60% survival at 168 hours [1]. Olive oil is composed of different polyunsaturated fatty acids such as omega 3 and 6, but the monounsaturated fatty acid omega 9, also known as oleic acid (OA), that is the main component of olive oil, is highly consumed in the Mediterranean diet.

Objective

We aim to investigate the role of OA in an experimental model of sepsis.

Methods

Swiss mice were given daily doses (orally) of OA, at 282 μg/animal, for 15 days. Control animals received saline. On the 16th day, polymicrobial sepsis was induced by cecal ligation and puncture (CLP). Immediately after the procedure, all mice received volemic reposition and after 6 hours animals were given imipenem. Twenty-four hours after surgery, mice were euthanized and the peritoneal cavity was rinsed with sterile saline. Total leukocyte counts were performed in a Neubauer chamber and differential leukocyte were stained with May-Grunwald Giemsa. The supernatant and plasma were collected for cytokine quantification. In another set of experiments, the survival rate was determined daily for 7 days in separate groups of 10 animals for each condition.

Results

Mice fed with OA were resistant to sepsis, with a 64% survival rate at 168 hours compared with saline-treated mice (33%). OA supplementation in CLP-subject animals led to a significant decrease in the total leukocyte counts (10.69 × 10⁶ ± 1.71), mainly neutrophils, compared with mice that received saline (20.30 × 10⁶ ± 2.69). However, in mice that consumed OA the levels of TNFα, IL-10 and IL-6 were not significantly different from mice fed with saline submitted to CLP. Interestingly, preliminary data showed that mice fed with OA had a lower level of bacteria in the peritoneal lavage leukocyte compared with mice submitted to CLP. See Figure 1.

Figure 1

Bacterial count in the peritoneal lavage leukocyte is lower in oleic acid-treated mice submitted to CLP.

Conclusions

Our data suggest that treatment with OA reduces mortality in an experimental model of sepsis and attenuates inflammation. One mechanism involved may be due to an increased bacterial clearance in mice fed with OA. More data are required to clarify this mechanism of increased survival.