Sex differences in postprandial plasma tumor necrosis factor-alpha, interleukin-6, and C-reactive protein concentrations.

Abdominal obesity and insulin resistance are characterized by low-level chronic inflammation most likely implicated in the increased cardiovascular disease risk associated with these conditions. However, not much is known of the acute regulation of circulating inflammatory markers in response to food intake. The aim of this study is to examine changes in inflammatory marker concentrations after the consumption of a high-fat meal in men and women. We measured tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and C-reactive protein concentrations in plasma samples collected at 0, 4, and 8 hours after consumption of the meal in 39 men and 41 women. Associations between these variations and physical as well as metabolic variables were then examined. We noted significant increases in plasma IL-6 concentrations at 4 and 8 hours after the meal in men (+34% and +107%, respectively; P < .005 vs 0 hour) and women (+78% and +153%, respectively; P < .0001 vs 0 hour). Postprandial plasma TNF-alpha concentrations significantly dropped at 4 hours after the high-fat meal in men (-9.5%, P < .0005 vs 0 hour) and women (-5.5%, P < .05 vs 0 hour). Plasma CRP concentrations were not affected by food intake in either men or women. We also found that postprandial plasma concentrations of IL-6 were lower in subjects with a normal glucose tolerance (n = 69) compared with individuals with an impaired glucose tolerance (n = 11). Results of the present study show that consumption of a high-fat meal is associated with a transient reduction in circulating concentrations of TNF-alpha in both men and women as well as an elevation of plasma IL-6 concentrations that was found to be greater in women than in men.

Bacterial cyclic beta-(1,2)-glucan acts in systemic suppression of plant immune responses.

Although cyclic glucans have been shown to be important for a number of symbiotic and pathogenic bacterium-plant interactions, their precise roles are unclear. Here, we examined the role of cyclic beta-(1,2)-glucan in the virulence of the black rot pathogen Xanthomonas campestris pv campestris (Xcc). Disruption of the Xcc nodule development B (ndvB) gene, which encodes a glycosyltransferase required for cyclic glucan synthesis, generated a mutant that failed to synthesize extracellular cyclic beta-(1,2)-glucan and was compromised in virulence in the model plants Arabidopsis thaliana and Nicotiana benthamiana. Infection of the mutant bacterium in N. benthamiana was associated with enhanced callose deposition and earlier expression of the PATHOGENESIS-RELATED1 (PR-1) gene. Application of purified cyclic beta-(1,2)-glucan prior to inoculation of the ndvB mutant suppressed the accumulation of callose deposition and the expression of PR-1 in N. benthamiana and restored virulence in both N. benthamiana and Arabidopsis plants. These effects were seen when cyclic glucan and bacteria were applied either to the same or to different leaves. Cyclic beta-(1,2)-glucan-induced systemic suppression was associated with the transport of the molecule throughout the plant. Systemic suppression is a novel counterdefensive strategy that may facilitate pathogen spread in plants and may have important implications for the understanding of plant-pathogen coevolution and for the development of phytoprotection measures.