Allergic march in children of Ukraine

Allergic diseases, which have a certain stage in their development from food allergy to bronchial asthma / allergic rhinitis, are much more common in children than in adults. The aim of this study was to analyze data on the prevalence and incidence of atopic dermatitis, bronchial asthma and allergic rhinitis as components of the allergic march, in children of Ukraine from 1994 to 2017 to determine the possible impact of adverse environmental factors on their development. During the same period, due to the influence of a number of factors, in particular environmental, there were significant changes in the structure of allergic diseases making up the stages of the allergic march due to an increase in the proportion of allergic rhinitis with the reduced one of asthma and atopic dermatitis. Within 24 years, the incidence of atopic dermatitis in children aged 0-6 years including, increased by 27.6%, in adolescents - by 40.5% and significantly decreased by 39.5% in children aged 7-14 years including. Most cases of allergic rhinitis and bronchial asthma were observed in schoolchildren (47.6 and 54.0%, respectively) with a slight decrease compared to 1994. In general, allergic diseases in recent years have become more common in children from 0 to 6 years and their detection has decreased in school-age children and adolescents. Over the past 24 years, in children of Ukraine a steady increase in the incidence and prevalence of allergic diseases that form an allergic march has been noted: the prevalence of bronchial asthma has increased by 69.3% and the incidence has increased by 22.9%; the prevalence of atopic dermatitis increased by 43.9% and the incidence increased by 8.3%; the prevalence of allergic rhinitis increased by 488.3% and the incidence of allergic rhinitis increased by 380.3%, with a predominance of detection of this pathology in children from regions with developed infrastructure and industry, where there are significant emissions of pollutants into the atmosphere, that have a direct moderate effect on the increase in the prevalence of bronchial asthma, the incidence and prevalence of allergic rhinitis in children.

Can a gut helminth parasite influence Th2 inflammatory responses in the skin?

<p>Helminth parasites are one of the most common infectious agents of humans and cause significant health and economic burdens in the countries they are endemic in, making elimination an important goal. However, epidemiological studies have suggested an inverse correlation between the incidences of infections by helminth parasites in humans and autoimmune and allergic disease prevalence worldwide; it is thought the eradication of parasites in more affluent countries through improved hygiene is an important factor for the increasing incidence of autoimmune and allergic diseases encountered in the Western world. A Th2 immune response is central in providing immunity against helminth parasites, while suppressing T helper (Th) 1/Th17-mediated inflammation and inducing wound repair mechanisms. Helminths have developed strategies to directly regulate the immune response against them to ensure their own survival. Experimental evidence has demonstrated helminths are also able to dampen inflammatory bystander immune responses in their host, via induction of regulatory mechanisms such as regulatory T cells. These studies have focused primarily on the suppression of food and airway allergies in mouse models and there is limited data on the effect of helminth parasites on skin allergy e.g. atopic dermatitis. Atopic dermatitis (AD) is a chronic/chronically relapsing Th2 inflammatory skin condition, characterized by skin lesions, dry itchy skin and impaired skin barrier function. This is believed to allow the entrance of other allergens into the body more easily, leading to sensitization and initiation of other allergies later in life, a process termed the ‘Allergic March’. With the increased incidence of allergy in the Western world, it is desirable to find new therapies to suppress AD and the onset of the allergic march. During my Masters, I have investigated whether the gut-dwelling mouse parasite Heligmosomoides polygyrus was able to suppress Th2 responses induced in skin tissue using two different allergy models: 1) intradermal injection (ID) of whole mashed-up house dust mite (HDM), which induces Th2 inflammatory responses, and 2) topical application of the chemical hapten dibutyl phthalate-fluorescein isothiocyanate (DBP-FITC), mimicking allergic responses seen in AD. The results show that H. polygyrus induces interleukin (IL)-4 production in tissues distal to the gut, including the ear skin tissue, mainly from cluster of differentiation (CD) 4⁺ T cells. Furthermore, helminth infection was able to suppress Th2-mediated inflammation in the skin in both house dust mite and DBP-FITC models, coinciding with an increase in the proportions of regulatory T cells (Tregs) in skin-associated lymph nodes (LNs). This research further demonstrates the potential use of helminth parasites, or their products, as a therapy for allergic diseases, including those of the skin.</p>

Can a gut helminth parasite influence Th2 inflammatory responses in the skin?

<p>Helminth parasites are one of the most common infectious agents of humans and cause significant health and economic burdens in the countries they are endemic in, making elimination an important goal. However, epidemiological studies have suggested an inverse correlation between the incidences of infections by helminth parasites in humans and autoimmune and allergic disease prevalence worldwide; it is thought the eradication of parasites in more affluent countries through improved hygiene is an important factor for the increasing incidence of autoimmune and allergic diseases encountered in the Western world. A Th2 immune response is central in providing immunity against helminth parasites, while suppressing T helper (Th) 1/Th17-mediated inflammation and inducing wound repair mechanisms. Helminths have developed strategies to directly regulate the immune response against them to ensure their own survival. Experimental evidence has demonstrated helminths are also able to dampen inflammatory bystander immune responses in their host, via induction of regulatory mechanisms such as regulatory T cells. These studies have focused primarily on the suppression of food and airway allergies in mouse models and there is limited data on the effect of helminth parasites on skin allergy e.g. atopic dermatitis. Atopic dermatitis (AD) is a chronic/chronically relapsing Th2 inflammatory skin condition, characterized by skin lesions, dry itchy skin and impaired skin barrier function. This is believed to allow the entrance of other allergens into the body more easily, leading to sensitization and initiation of other allergies later in life, a process termed the ‘Allergic March’. With the increased incidence of allergy in the Western world, it is desirable to find new therapies to suppress AD and the onset of the allergic march. During my Masters, I have investigated whether the gut-dwelling mouse parasite Heligmosomoides polygyrus was able to suppress Th2 responses induced in skin tissue using two different allergy models: 1) intradermal injection (ID) of whole mashed-up house dust mite (HDM), which induces Th2 inflammatory responses, and 2) topical application of the chemical hapten dibutyl phthalate-fluorescein isothiocyanate (DBP-FITC), mimicking allergic responses seen in AD. The results show that H. polygyrus induces interleukin (IL)-4 production in tissues distal to the gut, including the ear skin tissue, mainly from cluster of differentiation (CD) 4⁺ T cells. Furthermore, helminth infection was able to suppress Th2-mediated inflammation in the skin in both house dust mite and DBP-FITC models, coinciding with an increase in the proportions of regulatory T cells (Tregs) in skin-associated lymph nodes (LNs). This research further demonstrates the potential use of helminth parasites, or their products, as a therapy for allergic diseases, including those of the skin.</p>

Allergy-Related Symptoms Are Poorly Predicted by IgE and Skin Prick Testing in Early Life

<b><i>Introduction:</i></b> In childhood, the so-called allergic march involves progression from IgE sensitization to allergy-related symptoms. Both IgE sensitization and relevant clinical symptoms are required for the diagnosis of allergy, but concordance between test results and clinical symptoms varies greatly, creating challenges for the diagnostics and for the prediction of outcomes. We assessed the prevalence of IgE sensitization and allergy symptoms, concordance between 2 IgE sensitization testing methods, and predictive value of these tests in relation to clinical symptoms in young Finnish children. <b><i>Methods:</i></b> The current study included 2 series of children: a birth cohort, in which the participants were followed prospectively from birth up to 3 years, and a young children cohort observed from 3 to 5 years of age. They were regularly monitored for sensitization by measuring serum allergen-specific IgEs (sIgEs) and performing skin prick tests (SPTs). The emergence of atopic dermatitis, wheezing, and symptoms associated with food allergies was recorded. <b><i>Results:</i></b> Over the first 5 years of life, the prevalence of sIgE sensitization was 46%, while it was 36% for positive SPTs. Disease prevalence was 26% for atopic dermatitis, 25% for wheezing, and 19% for symptoms associated with food allergies. Concordance between sIgE and SPT results was good for aeroallergens, but poor for dietary allergens. The association between clinical symptoms and sensitization was stronger at 5 years than at 3 years of age. The proportion of children with concordant combinations of allergy symptoms and sensitization markers in contrast to those with discordant combinations increased from 3 to 5 years. <b><i>Conclusion:</i></b> In early childhood, testing for IgE sensitization predicts allergy-related symptoms in an age-dependent manner, but not particularly well. Tests predict symptoms caused by aeroallergens clearly better than those caused by dietary allergens. The clinical relevance of sensitization testing in early life is therefore limited in the prediction of true allergy.

Asthma/Rhinitis (The United Airway) and Allergy: Chicken or Egg; Which Comes First?

While allergy, asthma and rhinitis do not inevitably co-exist, there are strong associations. Not all those with asthma are allergic, rhinitis may exist without asthma, and allergy commonly exists in the absence of asthma and/or rhinitis. This is likely due to the separate gene/environment interactions which influence susceptibility to allergic sensitization and allergic airway diseases. Allergic sensitization, particularly to foods, and eczema commonly manifest early in infancy, and not infrequently are followed by the development of allergic rhinitis and ultimately asthma. This has become known as the “allergic march”. However, many infants with eczema never develop asthma or rhinitis, and both the latter conditions can evolve without prior eczema or food allergy. Understanding the mechanisms underlying the ontogeny of allergic sensitization and allergic disease will facilitate rational approaches to the prevention and management of asthma and allergic rhinitis. Furthermore, a range of new, so-called biological, therapeutic approaches, targeting specific allergy-promoting and pro-inflammatory molecules, are now in clinical trials or have been recently approved for use by regulatory authorities and could have a major impact on disease prevention and control in the future. Understanding basic mechanisms will be essential to the employment of such medications. This review will explain the concept of the united airway (rhinitis/asthma) and associations with allergy. It will incorporate understanding of the role of genes and environment in relation to the distinct but interacting origins of allergy and rhinitis/asthma. Understanding the patho-physiological differences and varying therapeutic requirements in patients with asthma, with or without rhinitis, and with or without associated allergy, will aid the planning of a personalized evidence-based management strategy.