Food Allergies and Parasites in Children.

The dynamically growing incidence of food allergies forces the scientific community to develop new methods for their diagnosis, differentiation, and effective treatment. Parasitoses appear much less frequently in the scientific literature, as well as among the presumed causes of numerous conditions. The similarity of inflammatory mechanisms in allergies and parasitosis necessitates a revision of current diagnostic standards. A lack of specificity and the coincidence of symptoms at an early stage of disease can lead to misdiagnosis. In this paper, we attempted to perform a comparative analysis of the similarities and differences in symptoms for these two types of diseases. We described the molecular mechanisms and metabolic pathways of food allergy and parasitosis. We presented the available research methods and directions of ongoing studies aimed at implementing precise medical techniques for differential diagnosis. We discussed the allergenic properties of certain parasite proteins, using the example of myofibrillar tropomyosins from the nematode Anisakis simplex. The literature in the fields of allergology and parasitology leads to the conclusion that it is reasonable to run parallel allergological and parasitological diagnostics in patients with non-specific symptoms. This approach will facilitate accurate and early diagnosis and implementation of effective therapy.

Analysis of the Serum Profile of Cytokines Involved in the T-Helper Cell Type 17 Immune Response Pathway in Atopic Children with Food Allergy.

The main risk factor for the development of food allergies (FAs) in children is atopic dermatitis (AD). AD is usually recognized as the Th1/Th2 paradigm of allergic disease. Recently, the Th1/Th2 paradigm in allergy and autoimmunity has been revised, including the role of the Th17 cell population and related cytokines. However, there are only a few studies that have found Th17 cytokine involvement in the allergic inflammatory response, especially with food allergens. This research aimed to analyze the serum profile of cytokines involved in the T-helper cell type 17 immune response pathway in young, atopic children with an IgE-mediated and delayed-type FA. The study involved 76 children (0−5 years old) with chronic AD. We used the Bio-Plex system to simultaneously determine the concentrations of 15 different cytokines in one experiment. In accordance with complete dermatological and allergological examination, including OFC testing and ALEX2 assays, participants were divided into 3 groups: IgE-mediated FA, delayed-type FA, and the control group. Data were analyzed using univariate statistical tests. In the IgE-mediated FA group, the circulating levels of tested cytokines had increased compared with those of other patients; however, a statistically significant difference was only obtained for IL-1beta (p < 0.05). According to the ROC curves, IL-1beta may be considered an effective predictor of IgE-mediated FA in AD children (p < 0.05; AUC = 0.67). In the delayed-type FA group, the concentration of most cytokines had slightly decreased compared to the control group. The obtained results suggest that FA influences the Th17-related cytokine profile in the serum of AD children. More advanced studies are needed to confirm the involvement of Th17 cytokines in the allergic inflammatory response and to prove their usefulness in clinical practice.

Is Vitamin D Deficiency Related to Increased Cancer Risk in Patients with Type 2 Diabetes Mellitus?

There is mounting evidence that type 2 diabetes mellitus (T2DM) is related with increased risk for the development of cancer. Apart from shared common risk factors typical for both diseases, diabetes driven factors including hyperinsulinemia, insulin resistance, hyperglycemia and low grade chronic inflammation are of great importance. Recently, vitamin D deficiency was reported to be associated with the pathogenesis of numerous diseases, including T2DM and cancer. However, little is known whether vitamin D deficiency may be responsible for elevated cancer risk development in T2DM patients. Therefore, the aim of the current review is to identify the molecular mechanisms by which vitamin D deficiency may contribute to cancer development in T2DM patients. Vitamin D via alleviation of insulin resistance, hyperglycemia, oxidative stress and inflammation reduces diabetes driven cancer risk factors. Moreover, vitamin D strengthens the DNA repair process, and regulates apoptosis and autophagy of cancer cells as well as signaling pathways involved in tumorigenesis i.e., tumor growth factor ß (TGFß), insulin-like growth factor (IGF) and Wnt-ß-Cathenin. It should also be underlined that many types of cancer cells present alterations in vitamin D metabolism and action as a result of Vitamin D Receptor (VDR) and CYP27B1 expression dysregulation. Although, numerous studies revealed that adequate vitamin D concentration prevents or delays T2DM and cancer development, little is known how the vitamin affects cancer risk among T2DM patients. There is a pressing need for randomized clinical trials to clarify whether vitamin D deficiency may be a factor responsible for increased risk of cancer in T2DM patients, and whether the use of the vitamin by patients with diabetes and cancer may improve cancer prognosis and metabolic control of diabetes.