Intestinal microbial-derived sphingolipids are inversely associated with childhood food allergy.
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ABSTRACT:
SUBMITTER: Lee-Sarwar K
PROVIDER: S-EPMC6433125 | biostudies-literature | 2018 Jul
REPOSITORIES: biostudies-literature
Publications
Intestinal microbial-derived sphingolipids are inversely associated with childhood food allergy.
Lee-Sarwar Kathleen K Kelly Rachel S RS Lasky-Su Jessica J Moody D Branch DB Mola Alex R AR Cheng Tan-Yun TY Comstock Laurie E LE Zeiger Robert S RS O'Connor George T GT Sandel Megan T MT Bacharier Leonard B LB Beigelman Avraham A Laranjo Nancy N Gold Diane R DR Bunyavanich Supinda S Savage Jessica H JH Weiss Scott T ST Brennan Patrick J PJ Litonjua Augusto A AA
The Journal of allergy and clinical immunology 20180502 1
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Project description:BackgroundChildhood food allergy and asthma rates are increasing. The hygiene hypothesis has been proposed as an explanation for the increased incidence of allergic disease.ObjectiveTo describe the association of childhood food allergy and asthma with hygiene factors, such as the number of siblings, antibiotic use, infection history, pet exposure, child care exposure, and maternalchild factors.MethodsChildren ages 021 years old (N = 1359) were recruited for a cross-sectional family-based study, including children with food allergy and children without food allergy, and their siblings. We assessed the associations between childhood food allergy and asthma with hygiene factors.ResultsOf the 1359 children, 832 (61.2%) had food allergy, and 406 (30%) had asthma. In the adjusted analysis, the prevalence of food allergy was increased if there was a history of skin infection (prevalence ratio [RRR] 1.12 [95% confidence interval {CI}, 1.011.24]) or eczema (RRR 1.89 [95% CI, 1.702.10]). The prevalence of asthma was increased with a history of respiratory syncytial virus infection (RRR 1.60 [95% CI, 1.341.90]) or eczema (RRR 1.54 [95% CI, 1.271.86]). A greater number of siblings were associated with a decreased prevalence of food allergy (RRR 0.79 [95% CI, 0.750.84]) and asthma (RRR 0.82 [95% CI, 0.740.91]).ConclusionOur findings supported the accumulating evidence of an association between skin infections and eczema with food allergy. Because these results could be subject to recall bias, additional prospective studies are needed to substantiate these findings.
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Project description:Food allergy (FA) is a significant public health issue, propelled by its rapidly increasing prevalence. Its sharp rise into prominence has focused attention on causative environmental factors and their interplay with the immune system in disease pathogenesis. In that regard, there is now substantial evidence that alterations in the gut microbiome early in life imprint the host gut mucosal immunity and may play a critical role in precipitating FA. These changes may impact key steps in the development of the infant gut microbiome, including its shaping by maternal factors and upon the introduction of solid food (the weaning reaction). These early-life changes may have long-range effects on host immunity that manifest later in time as disease pathology. Experimental studies have shown that resetting the host intestinal immune responses by treatment with either a healthy fecal microbiota transplantation or defined commensal bacterial taxa can prevent or treat FA. The mechanisms by which these interventions suppress FA include restoration of gut immune regulatory checkpoints, notably the retinoic orphan receptor gamma T+ regulatory T cells, the epithelial barrier, and healthy immunoglobulin A responses to the gut commensals. These findings inform human studies currently in progress that evaluate the role of microbial therapies in FA.
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Project description:Microbiota plays an important role in regulating immune responses associated with atopic diseases. We sought to evaluate relationships among airway microbiota, serum IgE levels, allergic sensitization and their relevance to rhinitis and asthma. Microbial characterization was performed using Illumina-based 16S rRNA gene sequencing of 87 throat swabs collected from children with asthma (n = 32) and rhinitis (n = 23), and from healthy controls (n = 32). Data analysis was performed using QIIME (Quantitative Insights Into Microbial Ecology) v1.8. Significantly higher abundance of Proteobacteria was found in children with rhinitis than in the healthy controls (20.1% vs. 16.1%, P = 0.009). Bacterial species richness (Chao1 index) and diversity (Shannon index) were significantly reduced in children with mite sensitization but not in those with food or IgE sensitization. Compared with healthy children without mite sensitization, the mite-sensitized children with rhinitis and asthma showed significantly lower Chao1 and Shannon indices. Moraxella and Leptotrichia species were significantly found in the interaction of mite sensitization with rhinitis and asthma respectively. Airway microbial diversity appears to be inversely associated with sensitization to house dust mites. A modulation between airway dysbiosis and responses to allergens may potentially cause susceptibility to rhinitis and asthma in early childhood.
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Project description:Background:The role of infant feeding for food allergy in children is unclear and studies have not addressed simultaneous exposures to different foods. The goal of this study was to analyze existing data on feeding practices that represent realistic exposure and assess the risk of food allergy symptoms and food allergy in children. Methods:The Infant Feeding Practices Study II conducted by the CDC and US-FDA enrolled pregnant women and collected infant feeding information using nine repeated surveys. Participants were re-contacted after 6 years. Food allergy data were collected at 4, 9, 12, and 72 months. In total, 1387 participants had complete infant feeding pattern data for 6 months and information on food allergy symptoms and doctors' diagnosed food allergy. Feeding patterns constituted six groups: 3-months of feeding at breast followed by mixed feeding, 3-months of breast milk and bottled milk followed by mixed feeding, 1-month of feeding at breast followed by mixed feeding, 6-months of mixed feeding i.e., concurrent feeding of breast milk, bottled milk and formula, 2-3 months of formula followed by formula and solid food, and formula and solid food since the first month. To estimate risks of food allergy, we used linear mixed models, controlling for potential confounders. Results:Of the 328 children with food allergy symptoms in infancy and at 6 years, 52 had persistent symptoms from infancy. Children exposed to mixed feeding had a higher risk of food allergy symptoms (Risk Ratio [RR] 1.54; 95% Confidence Interval [CI] 1.04, 2.29) compared to 3-months of feeding at breast adjusted for confounding. No statistically significant risk of infant feeding patterns was found for doctors' diagnosed food allergy. Paternal allergy posed a higher risk for food allergy symptoms (RR 1.36; 95% CI 1.01, 1.83). Prenatal maternal smoking increased the risk for doctors' diagnosed food allergy (RR 2.97; 95% CI 1.53, 5.79). Conclusions:Analysis of this prospective birth cohort suggest that introduction of multiple feeding source may lead to food allergy symptoms. Future efforts are needed to determine acceptable approaches to improve the ascertainment of food allergy in children and the role of infant feeding.
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Project description:BackgroundFilaggrin is an epidermal protein that has a role in skin barrier function. Filaggrin loss-of-function (FLG-LOF) mutations are a significant risk factor for eczema and atopy, but their association with food allergy (FA) is less clear.ObjectiveWe explored the longitudinal relationship between 3 common FLG-LOF mutations and FA using the Isle of Wight birth cohort.MethodsFA diagnosis was based on recognized allergic reactions within 4 hours after exposure to known food allergens. Food allergen sensitization (FAS) was identified by using skin prick tests conducted between 1 and 18 years of age to a range of food allergens. Three FLG mutations were genotyped in 1150 (79%) of 1456 children. The temporal relationships between FA, FAS, and eczema in children with FLG mutations were explored by using path analysis with total, direct, and indirect effect models.ResultsThere was a significant total effect of FLG-LOF mutations on the risk of FA in later childhood at the ages of 10 (odds ratio, 31.46; 95% CI, 2.86 to >100) and 18 (odds ratio, 4.25; 95% CI, 1.55-11.61) years. Path analysis showed that there was no direct effect of FLG-LOF mutations on FA at any age; however, an indirect effect was found on FA at all ages through eczema and FAS in the earlier years.ConclusionFLG-LOF mutations are associated with FA in older children through eczema and FAS during early childhood. Our results highlight a biologically plausible pathway, which suggests that skin barrier function is important in the development and persistence of FA.
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