Actinobacillus pleuropneumoniae is the causative agent of porcine contagious pleuropneumonia. Overproduction of proinflammatory cytokines, like interleukin-1β (IL-1β), IL-6, tumor necrosis factor alpha, and resistin, in the lung is an important feature of A. pleuropneumoniae infection. These proinflammatory cytokines enhance inflammatory and immunological responses. However, the mechanism that leads to cytokine production remains unclear. As a major virulence factor of A. pleuropneumoniae, lipopolysaccharide (LPS) may act as a potent stimulator of Toll-like receptor 4 (TLR4), triggering a number of intracellular signaling pathways that lead to the synthesis of proinflammatory cytokines. Porcine alveolar macrophages (PAMs) are the first line of defense against pathogenic microbes during pathogen invasion. The results of the present study demonstrate that A. pleuropneumoniae LPS induces PAMs to produce inflammatory cytokines in time- and dose-dependent manners. Moreover, PAMs were activated by A. pleuropneumoniae LPS, resulting in upregulation of signaling molecules, including TLR4, MyD88, TRIF-related adaptor molecule, and NF-κB. In contrast, the activation effects of A. pleuropneumoniae LPS on PAMs could be suppressed by specific inhibitors, like small interfering RNA and Bay11-7082. Taken together, our data indicate that A. pleuropneumoniae LPS can induce PAMs to produce proinflammatory cytokines via the TLR4/NF-κB-mediated pathway. These findings partially reveal the mechanism of the overproduction of proinflammatory cytokines in the lungs of swine with A. pleuropneumoniae infection and may provide targets for the prevention of A. pleuropneumoniae-induced pneumonia. All the data could be used as a reference for the pathogenesis of respiratory infection.

Diabetes mellitus is a heterogeneous, multifactorial, chronic disease characterized by hyperglycemia owing to insulin insufficiency and insulin resistance (IR). Recent epidemiological studies showed that the diabetes epidemic affects 382 million people worldwide in 2013, and this figure is expected to be 600 million people by 2035. Diabetes is associated with microvascular and macrovascular complications resulting in accelerated endothelial dysfunction (ED), atherosclerosis, and cardiovascular disease (CVD). Unfortunately, the complex pathophysiology of diabetic cardiovascular damage is not fully understood. Therefore, there is a clear need to better understand the molecular pathophysiology of ED in diabetes, and consequently, better treatment options and novel efficacious therapies could be identified. In the light of recent extensive research, we re-investigate the association between diabetes-associated metabolic disturbances (IR, subclinical inflammation, dyslipidemia, hyperglycemia, dysregulated production of adipokines, defective incretin and gut hormones production/action, and oxidative stress) and ED, focusing on oxidative stress and endothelial progenitor cells (EPCs). In addition, we re-emphasize that oxidative stress is the final common pathway that transduces signals from other conditions-either directly or indirectly-leading to ED and CVD.

The purpose of this study was to conduct a systematic review on the association of food patterns (FPs) and endothelial biomarkers. An electronic literature search from 1990 to 2012 was conducted and reference lists and experts were consulted. Studies without dietary intervention and without language restrictions were considered. Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were employed. Methodological quality was assessed by Strengthening the Reporting of Observational Studies in Epidemiology guidelines. A total of 546 references were identified, of which 8 were finally included. Several FPs were identified. Healthy FPs (abundant in fruits and vegetables) had a beneficial impact on endothelial function as estimated by circulating levels of biomarkers such as C-reactive protein, soluble intercellular adhesion molecule 1, soluble vascular adhesion molecule 1, and E-selectin molecules. Westernized patterns (higher intakes of processed meats, sweets, fried foods, and refined grains) were positively associated with inflammation molecules and atherogenic promoters. The study of FPs in relation to endothelial function contributes to the development of dietary recommendations for improved cardiovascular health and therefore a better lifestyle.

Hypoadiponectinemia and hyperresistinemia are associated with cardiovascular disease. The increase in the carotid intima-media thickness (CIMT) assessed by B-mode ultrasound has been directly associated with increased risk of myocardial infarction and stroke.

To evaluate the correlation between adipokine levels with CIMT in hypertensive type 2 diabetic patients.

Serum levels of adiponectin and resistin levels were measured by ELISA in 30 type 2 diabetic patients with never-treated hypertension and in age-matched healthy controls. The CIMT (B-mode color imaging of extracranial carotid arteries using high-resolution ultrasound) was also obtained. The relationship between adipokine levels and the adiponectin/resistin index with the CIMT was assessed by the Pearson correlation coefficient test.

Adiponectin was lower (p < 0.05), and resistin higher (p < 0.01) in patients than in controls, CIMT correlated positively with resistin (R = 0.45, p < 0.02) and the adiponectin/resistin index (R = 0.58, p < 0.001), but not with adiponectin levels (r = -0.11, p > 0.1) in patients. Whereas only adiponectin levels correlated - negatively - with CIMT (r = -0.39, p < 0.02) in controls.

Our results shown that the adiponectin/resistin index seems to be more strongly associated with atherosclerosis than adipokine levels, and may be used as a reliable marker of cardiovascular risk in type 2 diabetic hypertensive patients.

Oil thermoxidation during deep frying generates harmful oxidative free radicals that induce inflammation and increase the risk of hypertension. This study aimed to investigate the effect of repeatedly heated palm oil on blood pressure, aortic morphometry, and vascular cell adhesion molecule-1 (VCAM-1) expression in rats. Male Sprague-Dawley rats were divided into five groups: control, fresh palm oil (FPO), one-time-heated palm oil (1HPO), five-time-heated palm oil (5HPO), or ten-time-heated palm oil (10HPO). Feeding duration was six months. Blood pressure was measured at baseline and monthly using tail-cuff method. After six months, the rats were sacrificed and the aortic arches were dissected for morphometric and immunohistochemical analyses. FPO group showed significantly lower blood pressure than all other groups. Blood pressure was increased significantly in 5HPO and 10HPO groups. The aortae of 5HPO and 10HPO groups showed significantly increased thickness and area of intima-media, circumferential wall tension, and VCAM-1 than other groups. Elastic lamellae were disorganised and fragmented in 5HPO- and 10HPO-treated rats. VCAM-1 expression showed a significant positive correlation with blood pressure. In conclusion, prolonged consumption of repeatedly heated palm oil causes blood pressure elevation, adverse remodelling, and increased VCAM-1, which suggests a possible involvement of inflammation.

Adipokines have been implicated in the pathogenesis of atherosclerosis via pro-inflammatory mechanisms contributing to insulin resistance. The adipokine resistin causes endothelium dysfunction, which plays an important role in sustaining atherogenesis. This study investigated whether resistin induced expression of cell adhesion molecules and integrins in endothelial cells and THP-1 monocytes and whether such induction was attenuated by 1-20 μM caffeic acid. Resistin enhanced endothelial expression of vascular cell adhesion molecule 1 (VCAM-1), intercellular cell adhesion molecule 1 (ICAM-1), and E-selectin and monocyte expression of β1, β2, and α4 integrins. The enhancement of these proteins was diminished by caffeic acid with reduced THP-1 cell adhesion on activated endothelium. Caffeic acid at ≤20 μM demoted resistin-stimulated interleukin 8 (IL-8) production responsible for ICAM-1 and β2 integrin induction. The endothelial up-regulation of IL-8 secretion by resistin entailed toll-like receptor 4 (TLR4) activation, but caffeic acid diminished IL-8 production and TLR4 induction. Furthermore, caffeic acid encumbered resistin-activated nuclear factor κB (NF-κB) signaling. These results demonstrate that caffeic acid blocked monocyte trafficking to resistin-activated endothelium via disturbing NF-κB signaling responsive to IL-8. Therefore, caffeic acid may have therapeutic potential in preventing obesity-associated atherosclerosis.