Development Of Childhood Allergic Diseases Research Articles

Atopic March or Atopic Multimorbidity-Overview of Current Research.

The atopic march encompasses a sequence of allergic conditions, including atopic dermatitis, food allergy, allergic rhinitis, and asthma, that frequently develop in a sequential pattern within the same individual. It was introduced as a conceptual framework aimed at elucidating the developmental trajectory of allergic conditions during childhood. Following the introduction of this concept, it was initially believed that the atopic march represented the sole and definitive trajectory of the development of allergic diseases. However, this perspective evolved with the emergence of new longitudinal studies, which revealed that the evolution of allergic diseases is far more intricate. It involves numerous immunological pathological mechanisms and may not align entirely with the traditional concept of the atopic march. The objective of our review is to portray the atopic march alongside other patterns in the development of childhood allergic diseases, with a specific emphasis on the potential for a personalized approach to the prevention, diagnosis, and treatment of atopic conditions.

Effect of environmental exposures on allergen sensitization and the development of childhood allergic diseases: A large-scale population-based study

BackgroundChanging environmental factors are likely responsible for the rising prevalence of allergic diseases in children. However, whether environmental exposures induce allergen sensitizations, and which allergen sensitization is related to the development of allergic diseases, is not clear. The study is aimed to investigate the association between environmental exposure, allergen sensitization, and the development of allergic diseases for further preventive intervention. MethodsWe conducted the Taiwan Childhood Environment and Allergic diseases Study (TCEAS) in kindergarten children in Taiwan. Skin prick tests for 6 allergens were performed. Information on the development of allergic diseases and environmental exposure was collected using standardized questionnaires. Multiple logistic regressions were used to estimate the association between environmental factors, allergen sensitization, and the development of allergic diseases. ResultsA total of 3192 children were recruited. 485 (15.2%) children had atopic dermatitis (AD), 1126 (35.3%) had allergic rhinitis (AR), and 552 (17.3%) had asthma. Children with environmental tobacco smoke exposure and fungi on the house wall had a higher risk of asthma, with ORs (95% CIs) of 1.25 (1.03–1.52) and 1.22 (1.01–1.47), respectively. The mite sensitization rate was found to be the highest. Mite sensitization was associated with significant increases in the risks of AD, AR, and asthma, with ORs (95% CIs) of 2.15 (1.53–3.03), 1.94 (1.46–2.58), and 2.31 (1.63–3.29), respectively. Cockroach sensitization also increased the risk of asthma, with an OR (95% CI) of 2.38 (1.01–5.61). Mite sensitization was associated with carpet in the home and fungi on the house wall, and milk sensitization was associated with breastfeeding duration. ConclusionEnvironmental exposures play a role in the development of allergic diseases. Allergen sensitizations were associated with certain environmental exposures. Early environmental interventions are urgently needed to prevent the development of childhood allergic diseases.

Prenatal and neonatal factors involved in the development of childhood allergic diseases in Guangzhou primary and middle school students

BackgroundAllergic diseases, such as asthma, dermatitis, rhinitis, and eczema, are highly prevalent in Chinese school children. Environmental factors, including air pollution and automobile exhaust, play an important role in the etiology of these diseases. However, prenatal and neonatal factors, such as gender, maternal diseases during pregnancy, and premature birth, may also be associated with allergic disease occurrence. The objective of this study was to explore prenatal and neonatal factors that are involved in the development of allergic diseases among primary and middle school students in Guangzhou, China.MethodsA cross-sectional survey was launched by the Health Promotion Centre for Primary and Secondary Schools of the Guangzhou Municipality in October 2017. All primary and middle school students in Guangzhou were notified to participate in the questionnaire online under the direction of their parents. The results of the physical examination were reported by the schools’ medical department. The results of the questionnaire were collected and analyzed by the researchers. The prevalence of asthma, allergic rhinitis, allergic dermatitis, and eczema was identified.ResultsBased on reported 183,449 questionnaires and medical records, the data indicate that the sex, birth weight, neonatal feeding type, delivery mode, and students’ father smoking status were significantly associated with the prevalence of all four allergic diseases in primary and middle school children. In further stratified analyses of the children with normal birth weight (2500–4000 g) and without any maternal diseases during pregnancy, the factors of male sex, high birth weight, cesarean delivery, and father smoking status all increased the risk of asthma, dermatitis, rhinitis, and eczema. Also, unlike exclusive breastfeeding, breast plus formula feeding increased these risks, but pure formula feeding had the opposite effect.ConclusionPrenatal and neonatal factors, including male sex, high birth weight, cesarean delivery, only child, and father smoking status are associated with the risks of allergic diseases in school children.

Prenatal Diet and the Development of Childhood Allergic Diseases: Food for Thought.

The development of allergic disease is shaped by genetics and the environment, including diet. Many studies suggest a role for maternal diet during pregnancy. In this article, we discuss potential mechanisms by which specific nutrients, particular foods, and dietary patterns may influence allergic disease development and review studies examining the relationship between prenatal diet and the risk of childhood allergy. The combination of in utero exposures and genetic predisposition may contribute to the development of allergic disease by altering immune and organ development. Inflammation predominates in the first and third trimesters whereas the second trimester is characterized by anti-inflammatory and Th2 immune responses. Maternal dietary exposures during pregnancy may interact with inherited genetic risk factors influence immune system development. There are varied results regarding the impact of maternal prenatal diet on the development of childhood allergies. Well-designed randomized controlled studies are needed to clarify this area.

Exposure to outdoor air pollution during trimesters of pregnancy and childhood asthma, allergic rhinitis, and eczema

BackgroundMounting evidence suggests that exposure to ambient air pollution is associated with the development of childhood allergic diseases, but the effect of prenatal exposure to air pollution on the risk of childhood asthma and allergy is unclear. ObjectivesWe evaluated the association between maternal exposure to outdoor air pollution during different trimesters of pregnancy and incidence of asthma, allergic rhinitis, and eczema in 2598 preschool children aged 3–6 years in China. MethodsChildren's lifetime incidence of allergic diseases was obtained using questionnaire. Individual exposure to outdoor air pollutants during trimesters of pregnancy was estimated by an inverse distance weighted (IDW) method based on the measured concentrations at monitoring stations. We used multiple logistic regression method to estimate the odds ratio (OR) of asthma, allergic rhinitis, and eczema for per interquartile range (IQR) increase in the exposure to air pollutant in each trimester, which was adjusted for the effect of other air pollutants and its effect in other trimesters by a multi-pollutant/trimester model. ResultsIncidence of asthma (6.8%), allergic rhinitis (7.3%), and eczema (28.6%) in children was associated with maternal exposure to traffic-related pollutant NO2 during entire pregnancy with OR (95% confidence interval [CI]) respectively 1.63 (0.99–2.70), 1.69 (1.03–2.77), and 1.37 (1.04–1.80). After adjustment for other pollutants and trimesters, we found the association was significant only in specific trimester: the first trimester for eczema (1.54, 1.14–2.09), the second trimester for asthma (1.72, 1.02–2.97), and the third trimester for allergic rhinitis (1.77, 1.09–2.89). Sensitivity analysis indicated that the trimester sensitive to the development of allergic diseases was stable. ConclusionMaternal exposure to traffic-related air pollutant NO2 during pregnancy, especially in specific trimesters, is associated with an increased risk of developing asthma, rhinitis, and eczema in children. Our results support the hypothesis that childhood allergic diseases originate in fetal life and are triggered by traffic-related air pollution in sensitive trimesters.

Impact of perinatal environmental tobacco smoke on the development of childhood allergic diseases.

Allergic diseases such as asthma, allergic rhinitis, atopic dermatitis, and food allergy, are most common chronic, noncommunicable diseases in childhood. In the past few decades, the prevalence has increased abruptly worldwide. There are 2 possible explanations for the rising prevalence of allergic diseases worldwide, that an increased disease-awareness of physician, patient, or caregivers, and an abrupt exposure to unknown hazards. Unfortunately, the underlying mechanisms remain largely unknown. Despite the continuing efforts worldwide, the etiologies and rising prevalence remain unclear. Thus, it is important to identify and control risk factors in the susceptible individual for the best prevention and management. Genetic susceptibility or environments may be a potential background for the development of allergic disease, however they alone cannot explain the rising prevalence worldwide. There is growing evidence that epigenetic change depends on the gene, environment, and their interactions, may induce a long-lasting altered gene expression and the consequent development of allergic diseases. In epigenetic mechanisms, environmental tobacco smoke (ETS) exposure during critical period (i.e., during pregnancy and early life) are considered as a potential cause of the development of childhood allergic diseases. However, the causal relationship is still unclear. This review aimed to highlight the impact of ETS exposure during the perinatal period on the development of childhood allergic diseases and to propose a future research direction.

Traffic-related air pollution as a risk factor for the development of childhood allergic diseases: the “Traffic, Asthma and Genetics” project

Background Inter-individual variability in associations between traffic-related air pollution and childhood allergic diseases may be explained by genetics and unexplored gene-environment interactions. We combined previously collected data from two Canadian (CAPPS, SAGE) and four European (BAMSE, PIAMA, GINI, LISA) birth cohorts to examine whether exposure to traffic-related air pollution interacts with a child’s genetic profile to impact the risk of developing childhood asthma, allergic rhinitis …

Environmental exposures and the development of childhood allergic diseases

Background: Environmental factors may play a role to the increment of allergic diseases.Since the onsets of allergic diseases are relatively early in life, identification of environmental factors a...

Increased regulatory T-cell numbers are associated with farm milk exposure and lower atopic sensitization and asthma in childhood

European cross-sectional studies have suggested that prenatal and postnatal farm exposure decreases the risk of allergic diseases in childhood. Underlying immunologic mechanisms are still not understood but might be modulated by immune-regulatory cells early in life, such as regulatory T (Treg) cells. We sought to assess whether Treg cells from 4.5-year-old children from the Protection against Allergy: Study in Rural Environments birth cohort study are critical in the atopy and asthma-protective effect of farm exposure and which specific exposures might be relevant. From 1133 children, 298 children were included in this study (149 farm and 149 reference children). Detailed questionnaires until 4 years of age assessed farming exposures over time. Treg cells were characterized as upper 20% CD4(+)CD25(+) forkhead box protein 3 (FOXP3)(+) (intracellular) in PBMCs before and after stimulation (with phorbol 12-myristate 13-acetate/ionomycin or LPS), and FOXP3 demethylation was assessed. Atopic sensitization was defined by specific IgE measurements; asthma was defined by a doctor's diagnosis. Treg cells were significantly increased in farm-exposed children after phorbol 12-myristate 13-acetate/ionomycin and LPS stimulation. Exposure to farm milk was defined as a relevant independent farm-related exposure supported by higher FOXP3 demethylation. Treg cell (upper 20% CD4(+)CD25(+), FOXP3(+) T cells) numbers were significantly negatively associated with doctor-diagnosed asthma (LPS stimulated: adjusted odds ratio, 0.26; 95% CI, 0.08-0.88) and perennial IgE (unstimulated: adjusted odds ratio, 0.21; 95% CI, 0.08-0.59). Protection against asthma by farm milk exposure was partially mediated by Treg cells. Farm milk exposure was associated with increased Treg cell numbers on stimulation in 4.5-year-old children and might induce a regulatory phenotype early in life, potentially contributing to a protective effect for the development of childhood allergic diseases.

Acetaminophen and/or antibiotic use in early life and the development of childhood allergic diseases

Our understanding of whether the use of acetaminophen and/or antibiotics in early life can cause allergic diseases in later childhood remains inconclusive. The objective of this study was to investigate the temporal relationship between exposure to acetaminophen and/or antibiotics in early life and the development of allergic diseases in later childhood, using two independent birth cohorts derived from the National Health Insurance Research Database (NHIRD) in Taiwan. The authors conducted a prospective birth cohort study of 263 620 children born in 1998 and 9910 children born in 2003, separately, from the NHIRD. Exposure status of acetaminophen and/or antibiotics and potential confounding factors were included in the analyses. Cox proportional hazards models were applied to determine the temporal relationship between acetaminophen and/or antibiotic exposure and the development of allergic diseases. We observed a positive relationship between acetaminophen and/or antibiotic exposure during the 1st year of life and the subsequent development of the three examined allergic diseases (atopic dermatitis, asthma and allergic rhinitis) in the 1998 birth cohort, but the observed relationship of drug exposure in the 2003 cohort, especially for atopic dermatitis and asthma, was lower than for those in the 1998 cohort and was not statistically significant. Our findings provide suggestive evidence that the temporal effect of exposure to acetaminophen and/or antibiotics influences the development of common allergic diseases in later childhood. Further functional studies and/or animal studies are needed to better understand the underlying regulatory mechanisms driving this important clinical and public health issue.

Impairment of T-regulatory cells in cord blood of atopic mothers

Maternal atopy is a strong predictor for the development of childhood allergic diseases. The underlying mechanisms are ill defined, yet regulatory T (Treg) and T(H)17 cells may play a key role potentially shaping the early immune system toward a proallergic or antiallergic immune regulation. We examined T(H)1/T(H)2, Treg, and T(H)17 cell responses to innate (lipid A/peptidoglycan) and mitogen/adaptive (phytohemagglutinin/Dermatophagoides pteronyssinus 1) immune stimulation in cord blood from offspring of atopic/nonatopic mothers. Cord blood mononuclear cells from 161 healthy neonates (59% nonatopic, 41% atopic mothers) were investigated regarding Treg and T(H)17 cells (mRNA/surface markers), suppressive function, and proliferation/cytokine secretion. Cord blood from offspring of atopic mothers showed fewer innate-induced Treg cells (CD4(+)CD25(+)high), lower mRNA expression of associated markers (glucocorticoid-induced tumor necrosis factor receptor-related protein/lymphocyte activation gene 3; P < .05), and a trend toward lower Forkhead box transcription factor 3 (Foxp3) expression. Treg cell function was impaired in mitogen-induced suppression of T effector cells in cord blood of offspring from atopic mothers (P = .03). Furthermore, IL-10 and IFN-gamma secretion were decreased in innate-stimulated cord blood of offspring from atopic mothers (P = .04/.05). Innate-induced IL-17 was independent of maternal atopy and highly correlated with IL-13 secretion. In offspring of atopic mothers, Treg cell numbers, expression, and function were impaired at birth. T(H)17 cells were correlated with T(H)2 cells, independently of maternal atopy.

The Comparative Role of Gene and Environment on the Development of Childhood Allergic Respiratory Diseases

ISEE-472 Objective: Both genetic heredity and environmental elicitation are considered determining factors for the development of childhood allergic diseases with their prevalence and morbidity increasing in most parts of the world. This investigation studied the relative significance of either factor on developing childhood allergic diseases. Material and Methods: Parents of 425 children identified from a previously established birth-cohort, aged 4 to 7 years old, were successfully interviewed by telephone for their indoor environmental conditions after child's birth and current health status of the children. Multiple logistic regression was applied afterwards to examine the associations between indoor exposures, and the development of childhood illness with adjustment for parents' atopic status. Results: Initial analysis showed that paternal atopic history was more critical than that of maternal's on developing childhood allergic diseases. Population was then divided into 4 groups by the presence of environmental risk factor and paternal atopic status (− −, + −, − +, + +); children without paternal atopic history and environmental exposure (− − group) were the reference group for comparison. Preliminary results suggested environmental factors, such as ever water damage at home, visible mold, incense burning, and pet at home, did not appear to impose significant risk without the presence of paternal atopic heredity (+ −) on the development of physician-diagnosed atopic asthma or allergic rhinitis. However, a statistically significant risk was identified for those children with paternal atopic history (− +), odds ratio (OR) = 1.85 ∼ 2.36 for atopic asthma, and OR = 2.17 ∼ 3.55 for allergic rhinitis. The degree of risk seemed to elevate for these children if the environmental risk was also concurrently present (+ +) as a significant OR became 2.24 ∼ 4.63 for allergic rhinitis. Conclusions: The current data analysis imply that genetic heredity can be a more dominant risk, whereas environment exposure may be more an aggravating factor, on the development of childhood allergic diseases in Taiwanese population.

Cord Blood IgE and Dietary Patterns are Implicated in the Development of Childhood Allergic Diseases

Cord Blood IgE and Dietary Patterns are Implicated in the Development of Childhood Allergic Diseases