Preeclampsia is Associated with lower Percentages of Regulatory T Cells in Maternal Blood

Objective: Immunological mechanisms are involved in the pathophysiology of preeclampsia. During pregnancy there is an increase in regulatory T (Treg) cells, which has an important role in regulating tolerance to the immunologically distinct fetus. We hypothesised that percentages of Treg cells are decreased in preeclamptic patients. Methods: Peripheral blood was obtained from 26 healthy pregnant controls and 18 preeclamptic patients. Treg cells were measured using flow-cytometry. Results: Women with pregnancies complicated by preeclampsia had significantly lower percentages of CD4(+)FOXP3(+) Treg cells. Conclusion: We conclude that a deficiency of regulatory T cells may play a role in the pathophysiology of preeclampsia

Viral mimic poly-(I:C) attenuates airway epithelial T cell suppressive capacity; implications for asthma

In allergen-sensitised asthmatic individuals, allergen-specific type-2 T-helper cells proliferate and secrete type-2 cytokines (e.g. interleukin (IL)-4, -5 and -13), driving the airway inflammatory response that gives rise to the clinical symptoms of asthma. Both early-life sensitisation to aeroallergens and lower respiratory viral infections are important environmental risk factors for developing asthma. Additionally, respiratory viral infections are the most common trigger for asthma exacerbations. Of interest, many asthma susceptibility genes are expressed in the airway epithelium [1], which forms the first continuous line of defence against inhaled environmental insults, including viruses and aeroallergens. Impaired immune regulation and failure to maintain tolerance to allergens is thought to contribute to allergic sensitisation. Asthma epithelium may be deficient in its innate immune defence against viral infections, resulting in increased viral replication upon rhinovirus infection compared to nonasthma-derived epithelial cultures [2]. Furthermore, there is evidence for loss of the mucosal immune barrier in asthma, with disruption of epithelial integrity [1, 3]. This may lead not only to increased permeability, but also to the release of pro-inflammatory mediators, specifically of cytokines that drive type-2 responses [3, 4]. We recently observed that the ability of allergens to disrupt epithelial barrier function is related to the development of type-2-mediated inflammation in asthma [5, 6]. Furthermore, we demonstrated that healthy murine lung epithelium is a potent inhibitor of T-cell proliferation and that this inhibition is lost upon viral infection [7]. It is unknown if this immune regulatory effect is displayed by human epithelium and is dysregulated in asthma. We hypothesise that changes in this regulatory effect translate into aberrant regulation of T-cell responses in asthma. We studied the epithelial regulation of T-cell proliferation and cytokine responses upon epithelial stimulation with a viral mimic, using co-culture of human T-cells and primary bronchial epithelial cells (PBECs) from healthy controls and asthma patients

The rate of intestinal glucose absorption is correlated with plasma glucose-dependent insulinotropic polypeptide concentrations in healthy men

Glucagon-like pepticle-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) both play a role in the control of glucose homeostasis, and GIP is implicated in the regulation of energy storage. The capacity of carbohydrates to induce secretion of these incretin hormones could be one of the factors determining the metabolic quality of different types of carbohydrates. We analyzed the correlation between the rate of intestinal absorption of (starch-derived) glucose and plasma concentrations of GLP-1 and GIP after ingestion of glucose and starchy foods with a different content of rapidly and slowly available glucose. In a crossover study, glucose, insulin, GLP-1, and GIP concentrations were monitored for 6 h after consumption of glucose, uncooked cornstarch (UCCS) or corn pasta in 7 healthy men. All test meals were naturally labeled with C-13. Using a primed, continuous D-[6,6-H-2(2)]glucose infusion, the rate of appearance of exogenous glucose (RaEx) was estimated, reflecting the rate of intestinal glucose absorption. GLP-1 concentrations increased significantly from 180 to 300 min after ingestion of UCCS, the starch product with a high content of slowly available glucose. A high GIP response in the early postprandial phase (15-90 min) occurred after consumption of glucose. There was a strong positive within-subject correlation between RaEx and GIP concentrations (r=0.73, P &lt;0.01) across the test meals. Rapidly and slowly digestible carbohydrates differ considerably in their ability to stimulate secretion of incretin hormones; the metabolic consequences of such differences warrant exploration.</p

An explorative study of in vivo digestive starch characteristics and postprandial glucose kinetics of wholemeal wheat bread

&lt;p&gt;&lt;b&gt;Background&lt;/b&gt;&lt;/p&gt; &lt;p&gt;Based on in vitro measurements, it is assumed that starch in wholemeal bread is rapidly digestible, which is considered to be less desirable for health.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Aim of the study&lt;/b&gt;&lt;/p&gt; &lt;p&gt;To evaluate the in vitro prediction, we characterized starch digestion of wholemeal wheat bread (WB) and postprandial glucose kinetics in healthy volunteers.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Methods&lt;/b&gt;&lt;/p&gt; &lt;p&gt;In a crossover study 4 healthy men ingested either intrinsically &lt;sup&gt;13&lt;/sup&gt;C-enriched WB (133 g) or glucose (55 g) in water. Plasma glucose and insulin concentrations were monitored during 6 h postprandially. Using a primed continuous infusion of D-[6,6-&lt;sup&gt;2&lt;/sup&gt;H2] glucose, the rate of systemic appearance of glucose was estimated (reflecting glucose influx) and the endogenous glucose production calculated.&lt;/p&gt; &lt;p&gt;&lt;b&gt;Results&lt;/b&gt;&lt;/p&gt; &lt;p&gt;The glucose influx rate after WB was comparable with that after glucose in the early postprandial phase (0–2 h) (&lt;i&gt;P&lt;/i&gt; = 0.396) and higher in the late postprandial phase (2–4 h) (&lt;i&gt;P&lt;/i&gt; = 0.005). Despite the same initial glucose influx rate the 0–2 h incremental area under the curve (IAUC) of insulin after WB was 41% lower than after glucose (&lt;i&gt;P&lt;/i&gt; = 0.037). Paradoxically endogenous glucose production after WB was significantly more suppressed than after glucose (0–2 h IAUC: &lt;i&gt;P&lt;/i&gt; = 0.015, 2–4 h IAUC: &lt;i&gt;P&lt;/i&gt; = 0.018).&lt;/p&gt; &lt;p&gt;&lt;b&gt;Conclusions&lt;/b&gt;&lt;/p&gt; &lt;p&gt;Starch in WB seems to be partly rapidly and partly slowly digestible. Postprandial insulin response and endogenous glucose production after WB ingestion might not solely be determined by the digestive characteristics of starch; other components of WB seem to affect glucose homeostasis. In vitro measurements might not always predict in vivo starch digestion precisely.&lt;/p&gt