However, based on the results of IL-10 mRNA expression, we can hypothesize that the regulatory T-cells could be transferred to the lymph nodes during Coxiella infection. During first contact with C. burnetii, PBMCs of healthy pregnant goats are capable of recognizing C. burnetii and activate their early immune response in vitro. Furthermore, PBMCs from infected goats showed an augmented AbMole BioScience pro-inflammatory cytokine mRNA expression compared to PBMCs of naive goats after C. burnetii stimulation, whereas the anti-inflammatory cytokine IL10 was down-regulated. The finding that PBMCs from goats that have previously had contact with C. burnetii react differently than naive PBMCs can be useful in future vaccine strategies. Finally, although the PBMC response as found in infected goats is strongly geared towards a pro-inflammatory state, the infection is not cleared and the goats will still suffer abortions and stillbirths. The strong inverse relationship between high density lipoprotein cholesterol levels and coronary heart disease has been known for over three decades. HDL’s role in reverse cholesterol transport has been hypothesized to inhibit atherogenesis, and has been thought to contribute to HDL’s role as a negative cardiovascular risk factor. Recent research also has highlighted other functional properties of HDL, including its anti-inflammatory and anti-oxidant activities, as additional mechanisms to reduce atherosclerosis. Low HDL cholesterol levels are also associated with development of type 2 diabetes mellitus. Inflammation has been suggested to be responsible for the reduction in HDL levels seen in the setting of insulin resistance and obesity. However, recent data have also highlighted antiinflammatory properties of HDL, suggesting HDL may improve insulin sensitivity. Apolipoprotein A-I is the main protein in HDL and contributes to the cholesterol efflux, anti-oxidant, and antiinflammatory potential of HDL. ApoA-I mimetic peptides are 18 amino acid peptides modeled after the amphipathic ahelical structure of apoA-I. The 4F peptide, the most widely studied mimetic, has been shown to promote cholesterol efflux, have anti-inflammatory properties, and to reduce atherosclerosis and adiposity in some murine models. Early phase trials of 4F use in humans have been reported. The majority of murine studies with the 4F mimetic peptide have been conducted in apolipoprotein E deficient mice, a common model of hyperlipidemia associated with development of premature atherosclerosis. The apoE model does not lend itself to the study of obesity or insulin resistance, whereas the Ldlr mouse, another common model of atherosclerosis, allows for the combined study of diet induced obesity, insulin resistance, and atherosclerosis. Thus further investigation of the effect of the 4F mimetic peptide in the Ldlr model is warranted. The purpose of the current study was to determine the effect of 4F mimetic peptide on atherosclerosis and obesity in Ldlr mice fed an obesogenic diet. We also determined the effect of either apoA-I overexpression or the 4F mimetic peptide on insulin resistance and inflammation. We used a previously validated model of diet-induced obesity to induce atherosclerosis and insulin resistance, i.e., male Ldlr mice fed a high fat high sucrose diet with added cholesterol. The L4F version of the peptide, synthesized using L amino acids, was used based on our previous studies. Further, despite our previous studies showing that apoA-I overexpression can reduce adipose tissue inflammation, our current data suggests this does not confer improvements in glucose tolerance. Our in vitro studies demonstrated a novel ability of L4F to mimic apoA-I function in adipocytes.