Food allergy:definitions, prevalence, diagnosis and therapy / 中华预防医学杂志

Food allergy is phenotypically an extremely heterogeneous group of diseases affecting multiple organs, sometimes in an isolated way, sometimes simultaneously, with the severity of reactions ranging from mild and local to full-blown anaphylaxis. Mechanistically, it is defined as a Th2-driven immune disorder in which food-specific IgE antibodies are at the basis of immediate-type adverse reactions. The sites of sensitization and symptoms do not necessarily overlap. Food allergy, which is the theme of this paper, is often confused with other adverse reactions to food of both animmune (e.g., celiac disease) and non-immune (e.g., lactose intolerance) nature. To reliably diagnose food allergy, a careful history (immediate-type reactions) needs to be complemented with demonstration of specific IgE (immune mechanism) and confirmed by an oral challenge. Co-factors such as exercise, medication, and alcohol may help trigger food allergy and further complicate accurate diagnosis. Where food extract-based diagnostic tests are poorly correlated to symptom severity, new generation molecular diagnostics that measure IgE against individual food allergens provide clinicians and patients with more reliable symptom severity risk profiles. Molecular diagnostics also support establishing whether food sensitization originates directly from exposure to food or indirectly (cross-reactivity) from pollen sensitization. Epidemiological surveys have indicated that allergy to peach primarily originates from peach consumption in Europe, whereas in China it is the result of primary sensitization to mugwort pollen, in both cases mediated by an allergen molecule from the same family. Epidemiological surveys give insight into the etiology of food allergy, the size of the problem (prevalence), and the risk factors involved, which together support evidence-based strategies for prevention. Over the past decade, food allergy has increased in the affluent world. Economic growth and urbanization in upcoming economies are likewise expected to lead to increased prevalence of food allergies, sometimes to different foods due to dietary habits. Molecular allergology and biotechnology now offer the possibility to combat the increasing burden of food allergy by developing safe immunotherapies for food allergy, using hypoallergenic mutant recombinant molecules. The first clinical trials to evaluate such approaches are underway. Last but not least, the identification and clinical risk characterization of a more and more complete list of food allergens additionally provides the allergenicity risk assessment of genetically modified foods a firmer basis.

Signaling transduction pathways involved in basophil adhesion and histamine release / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Little is known about basophil with respect to the different signaling transduction pathways involved in spontaneous, cytokine or anti-IgE induced adhesion and how this compares to IgE-dependent and IgE-independent mediator secretion. The purpose of the present study was to investigate the roles of beta1 and beta2 integrins in basophil adhesion as well as hosphatidylinositol 3-kinase (PI3K), src-kinases and extracellular signal regulated kinase (ERK) 1/2 in basophil adhesion and histamine release (HR).</p><p><b>METHODS</b>Basophils (purity of 10% - 50%) were preincubated with anti-CD29 or anti-CD18 blocking antibodies before used for adhesion study. Basophils were preincubated with the pharmacological inhibitors wortmannin, PP1, PD98059 before used for adhesion and HR study. Cell adherence to bovine serum albumin (BSA) or fibronectin (Fn) was monitored using cell associated histamine as a basophil marker and the histamine was measured by the glass fiber assay.</p><p><b>RESULTS</b>Basophil spontaneous adhesion to Fn was inhibited by anti-CD29. Interleukin (IL)-3, granulocyte/macrophage colony stimulating factor (GM-CSF) induced adhesion to BSA was inhibited by anti-CD18. Wortmannin at 1 micromol/L and PP1 at 20 micromol/L strongly interfered with, whereas PD98059 at 50 micromol/L weakly inhibited basophil spontaneous adhesion to Fn. One micromol/L wortmannin strongly inhibited IL-3, IL-5, GM-CSF and anti-IgE induced adhesion to BSA. PP1 at 20 micromol/L partly inhibited anti-IgE induced adhesion. Fifty micromol/L PD98059 marginally inhibited IL-5, weakly inhibited anti-IgE, partly inhibited GM-CSF induced adhesion. Wortmannin, PP1 and PD98059 inhibited anti-IgE (1:100 or 1:1000) induced basophil HR in a dose dependent manner. They inhibited calcium ionophore A23187 (10 micromol/L, 5 micromol/L) induced basophil HR in a dose dependent manner, but to different extend with PP1 being the most efficient.</p><p><b>CONCLUSIONS</b>Basophil spontaneous adhesion to Fn is mediated by beta1-integrins whereas cytokine induced adhesion to BSA is mediated by beta2-integrins. PI3K, src-kinases and ERK1/2 play distinct signaling roles in basophil adhesion and HR. PI3K is the key player while ERK1/2 is the weakest participant.</p>