Non-allergic Mothers Research Articles

Increased allergic inflammation and decreased lung insulin sensitivity in offspring of obese allergic mothers.

Epidemiological studies demonstrate that maternal obesity and maternal allergy are major risk factors for asthma in offspring. However, the impact of maternal allergy and obesity on offspring lung insulin signaling and allergen responsiveness is not known. To evaluate this, allergic and nonallergic female mice were fed a high-fat diet or low-fat diet from 7 wk before pregnancy until weaning. Neonatal pups were allergen-sensitized and allergen-challenged and then were assessed for obesity, insulin signaling, and allergic inflammation. Compared with pups of nonobese nonallergic mothers, allergen-challenged pups of obese nonallergic mothers, nonobese allergic mothers, and obese allergic mothers had bronchoalveolar lavage (BAL) eosinophilia, with the pups of obese allergic mothers having the highest BAL eosinophilia. These pups also had lower insulin-induced lung AKT phosphorylation, indicating a decrease in lung parenchymal insulin sensitivity. In cross-fostering experiments, allergen-challenged pups exposed to both pre- and postnatal obese allergic mothers had the highest level of BAL eosinophilia. Maternal obesity or allergy increased offspring serum allergen-specific IgE and interleukin-5 that was highest when the mother was both obese and allergic. Also, allergen-challenged pups exposed to both pre- and postnatal obese allergic mothers had the highest level of interleukin-5. In summary, offspring born to obese allergic mothers have decreased lung insulin sensitivity and increased lung allergic inflammation. Interestingly, our data also demonstrate that there is both a pregnancy and postpregnancy aspect of maternal allergy and obesity that enhances allergen responsiveness in offspring.

Lung microbial dysbiosis during early life promotes predisposition to allergic asthma.

Abstract Background: Allergic asthma is associated with lung microbial dysbiosis. We hypothesized that the microbiome from the lungs of allergy-predisposed mouse pups is sufficient to predispose pups to development of allergy. Allergic inflammation in pups of allergic dams is blocked by α-tocopherol supplementation of the dam during gestation and nursing, but it is unknown whether α-tocopherol alters microbial composition of the lung. Methodology: Mouse pups were predisposed to allergy by inducing allergy in the mothers. Microbiome was separated from the bronchoalveolar lavage (BAL) of pups of allergic and non-allergic mothers and transferred intranasally at postnatal day 4. 16S rRNA sequencing was performed on the Illumina MiSeq platform. Results: Compared to pups born to non-allergic dams and dams administered with a-tocopherol supplementation, mouse pups born to allergic dams had elevated abundance of several genera of the γ-Proteobacteria, Firmicutes, and Verrucomicrobia (p<0.05). There was decreased abundance of genera from Bacteroides, Firmicutes, and α-Proteobacteria (p<0.05). Transfer of lung microbiome from neonates of allergic dams to neonates of non-allergic dams was sufficient to confer responsiveness to allergen in the recipient pups. Neonates of allergic dams were not protected from development of allergy by transfer of donor lung microbiome from neonates of non-allergic dams or neonates of αT-supplemented allergic dams. The donor microbiome from pups of allergic mothers colonized the pup lung, suggesting that early life detrimental bacterial species persists. Conclusion: The lung microbiome from allergy-predisposed pups is dominant and sufficient for enhanced neonate responsiveness to allergen. Supported by grants from NIH (R01AI127695)

Dysbiotic lung microbial communities of neonates from allergic mothers confer neonate responsiveness to suboptimal allergen.

In humans and animals, offspring of allergic mothers have increased responsiveness to allergens. This is blocked in mice by maternal supplementation with α-tocopherol (αT). Also, adults and children with allergic asthma have airway microbiome dysbiosis with increased Proteobacteria and may have decreased Bacteroidota. It is not known whether αT alters neonate development of lung microbiome dysbiosis or whether neonate lung dysbiosis modifies development of allergy. To address this, the bronchoalveolar lavage was analyzed by 16S rRNA gene analysis (bacterial microbiome) from pups of allergic and non-allergic mothers with a basal diet or αT-supplemented diet. Before and after allergen challenge, pups of allergic mothers had dysbiosis in lung microbial composition with increased Proteobacteria and decreased Bacteroidota and this was blocked by αT supplementation. We determined whether intratracheal transfer of pup lung dysbiotic microbial communities modifies the development of allergy in recipient pups early in life. Interestingly, transfer of dysbiotic lung microbial communities from neonates of allergic mothers to neonates of non-allergic mothers was sufficient to confer responsiveness to allergen in the recipient pups. In contrast, neonates of allergic mothers were not protected from development of allergy by transfer of donor lung microbial communities from either neonates of non-allergic mothers or neonates of αT-supplemented allergic mothers. These data suggest that the dysbiotic lung microbiota is dominant and sufficient for enhanced neonate responsiveness to allergen. Importantly, infants within the INHANCE cohort with an anti-inflammatory profile of tocopherol isoforms had an altered microbiome composition compared to infants with a pro-inflammatory profile of tocopherol isoforms. These data may inform design of future studies for approaches in the prevention or intervention in asthma and allergic disease early in life.

β-Glucosylceramide From Allergic Mothers Enhances Offspring Responsiveness to Allergen.

In animals and humans, offspring of allergic mothers have increased responsiveness to allergen and the allergen-specificity of the offspring can be different than that of the mother. In our preclinical models, the mother's allergic responses influence development of the fetus and offspring by elevating numbers of cells in dendritic cell subsets. A major question is the identity of maternal factors of allergic mothers that alter offspring development of responsiveness to allergen. Lipids are altered during allergic responses and lipids are transported to the fetus for growth and formation of fetal membranes. We hypothesized that pro-inflammatory lipids, that are elevated in allergic mothers, are transported to the fetus and regulate fetal immune development. We demonstrate in this report that there was a significant 2-fold increase in β-glucosylceramides (βGlcCer) in allergic mothers, the fetal liver and her offspring. The βGlcCer were transported from mother's plasma, across the placenta, to the fetus and in breastmilk to the offspring. Administration of βGlcCer to non-allergic mothers was sufficient for offspring responses to allergen. Importantly, maternal administration of a clinically relevant pharmacological inhibitor of βGlcCer synthase returned βGlcCer to normal levels in the allergic mothers and her offspring and blocked the offspring increase in dendritic cell subsets and offspring allergen responsiveness. In summary, allergic mothers had increased βGlcCer that was transported to offspring and mediated increases in offspring DCs and responsiveness to allergen. These data have a significant impact on our understanding of mechanisms for development of allergies in offspring of allergic mothers and have the potential to lead to novel interventions that significantly impact risk for allergic disease early in life.

Human Milk Fatty Acid Composition of Allergic and Non-Allergic Mothers: The Ulm SPATZ Health Study.

The aim of this study was to determine the differences in human milk fatty acid composition in relation to maternal allergy within a large birth cohort study using statistical methods accounting for the correlations that exist in compositional data. We observed marginal differences in human milk fatty acid composition of allergic and non-allergic mothers. However, our results do not support the hypothesis that human milk fatty acid composition is influenced by allergy or that it differs between mothers with or without allergy. Observed differences in our results between transformed and untransformed fatty acid data call for re-evaluation of previous, as well as future, studies using statistical methods appropriate for compositionality of fatty acid data.

Maternal Allergy and the Presence of Nonhuman Proteinaceous Molecules in Human Milk.

Human milk contains proteins and/or protein fragments that originate from nonhuman organisms. These proteinaceous molecules, of which the secretion might be related to the mother’s allergy status, could be involved in the development of the immune system of the infant. This may lead, for example, to sensitization or the induction of allergen-specific tolerance. The aim of this study was to investigate the relation between maternal allergy and the levels of nonhuman proteinaceous molecules in their milk. In this study, we analysed trypsin-digested human milk serum proteins of 10 allergic mothers and 10 nonallergic mothers. A search was carried out to identify peptide sequences originating from bovine or other allergenic proteins. Several methods were applied to confirm the identification of these sequences, and the differences between both groups were investigated. Out of the 78 identified nonhuman peptide sequences, 62 sequences matched Bos taurus proteins. Eight peptide sequences of bovine -lactoglobulin had significantly higher levels in milk from allergic mothers than in milk from nonallergic mothers. Dietary bovine -lactoglobulin may be absorbed through the intestinal barrier and secreted into human milk. This seems to be significantly higher in allergic mothers and might have consequences for the development of the immune system of their breastfed infant.

Association of maternal allergy with human milk soluble CD14 and fatty acids, and early childhood atopic dermatitis.

This study aimed to investigate whether maternal allergy is associated with soluble CD14 (sCD14) and fatty acid composition in different stages of lactation and the onset of atopic dermatitis (AD) in early childhood. In total, 443 mother-child groups (445 children) were enrolled in the Prediction of Allergies in Taiwanese Children birth cohort study. Colostrum and mature milk at 2months postpartum (2-month HM) were collected from lactating mothers. Information regarding parental allergy histories and physician-diagnosed atopic diseases was obtained using age-specific questionnaires (0-2years). We compared sCD14 levels and the composition of 30 fatty acids in the colostrum and 2-month HM, respectively, between allergic and non-allergic mothers and between children with and without AD by the age of 2years. In total, 185 (41.8%) mothers presented with allergies, and 154 (34.6%) children had physician-diagnosed AD by the age of 2years. Both in the colostrum and 2-month HM of 289 lactating mothers, sCD14 levels were significantly lower in allergic mothers whose children presented with AD compared with children who did not (P=0.015 and 0.044, respectively). Among the children with AD who were born to non-allergic mothers, sCD14 levels were lower. However, the result was not statistically significant (P=0.376 and 0.264, respectively). Our data revealed the lack of associations between fatty acid composition and AD (P>0.05). Decreased sCD14 levels in the colostrum and 2-month HM were associated with AD at 2years of age, particularly among children born to mothers with allergies.

Early-Life Environmental Factors, IFN-γ Methylation Patterns, and Childhood Allergic Rhinitis

Background: While early-life risk factors are known to influence the risk of allergies, the biological mechanisms underlying this observation are unclear. The aim of this study was to examine whether DNA methylation in childhood could underlie the association between early-life risk factors and allergic rhinitis (AR). Methods: In total, 234 patients, aged 6 years, were recruited, i.e., 114 were patients with AR (AR group) and 120 healthy children without AR (NAR group). The DNA methylation patterns of the IFN-γ promoter regions in CD4+ cells were analyzed using bisulfite sequencing. The percentage of Th1 was investigated by flow cytometry. The relationship among DNA methylation, early-life environment, and AR was examined. Results: After adjusting for several likely confounders, there was a higher likelihood of AR in children who had mothers with allergies than in children who had nonallergic mothers (OR = 5.19; 95% CI 1.18–29.41), in children who were born in autumn or winter than in children who were born in the summer or spring (OR = 2.69; 95% CI 1.34–5.40), and in children who lived with indoor carpet or wallpaper than in children who lived without indoor carpet or wallpaper (OR = 4.14; 95% CI 2.05–8.30). Compared to the NAR group, the AR group had higher mean methylation levels of the promoter region in IFN-γY, and lower numbers of IFN-γ+CD4+ cells were associated with autumn-winter birthdates. The season of birth had an indirect effect on AR at 6 years, which was mediated by the mean IFN-γ promoter methylation level. Conclusions: This study suggests that early-life environments affect AR, and this is supported by the finding of IFN-γY methylation as a mediator of the effect of an individual’s season of birth on AR.

Maternal Lipid Regulation of the Development of Responsiveness to Allergen in Neonates and Infants.

Abstract In animals and humans, offspring of allergic mothers have increased responsiveness to allergen. A major question is what are the maternal factors of allergic mothers that alter offspring responsiveness to allergen? We focused on maternal lipids, because lipids are altered during allergic inflammation and because lipids are transported to the fetal liver and are in the mother’s milk. In our studies, allergic pregnant mice had increased glucosylceramides (GlcCer) in the mother plasma, placenta, and fetal liver as compared to non-allergic mothers. In allergen-challenged pups of allergic mothers, GlcCer was elevated in the pup lung and liver. Maternal GlcCer is directly transported to the placenta, the fetal liver, mother breast tissue and the milk of the pup stomach. Administration of a pharmacolgical inhibitor of GlcCer synthase to allergic mothers reduced GlcCer to the levels of GlcCer in non-allergic mothers and blocked the development of allergic lung inflammation and generation of allergen-specific IgE in allergen-challenged pups of allergic mothers. We also demonstrated that the fetal liver and offspring of allergic mothers have increased numbers of resident dendritic cells (DCs) and that the administration of the GlcCer synthase inhibitor to the allergic mothers blocked the increase in these DCs in the offspring. In summary, allergic mothers had increased GlcCer that is transferred to offspring and mediates changes in offspring DCs and responsiveness to allergen. These data have a significant impact on our understanding of mechanisms of maternal lipid regulation of offspring development of allergies and has the potential to lead to novel interventions that significantly impact risk for allergic disease early in life.

Maternal diet during pregnancy and lactation and cow's milk allergy in offspring.

Diet during pregnancy and lactation may have a role in the development of allergic diseases. There are few human studies on the topic, especially focusing on food allergies. We sought to study the associations between maternal diet during pregnancy and lactation and cow's milk allergy (CMA) in offspring. A population-based birth cohort with human leukocyte antigen-conferred susceptibility to type 1 diabetes was recruited in Finland between 1997 and 2004 (n=6288). Maternal diet during pregnancy and lactation was assessed by a validated, 181-item semi-quantitative food frequency questionnaire. Register-based information on diagnosed CMA was obtained from the Social Insurance Institution and completed with parental reports. The associations between maternal food consumption and CMA were assessed using logistic regression, comparing the highest and the lowest quarters to the middle half of consumption. Consumption of milk products in the highest quarter during pregnancy was associated with a lower risk of CMA in offspring (odds ratio (OR) 0.56, 95% confidence interval (CI) 0.37-0.86; P<0.01). When stratified by maternal allergic rhinitis and asthma, there was evidence of an inverse association between high use of milk products and CMA in offspring of non-allergic mothers (OR 0.30, 95% CI 0.13-0.69, P<0.001). Cord blood IgA correlated positively with the consumption of milk products during pregnancy, indicating exposure to CMA and activation of antigen-specific immunity in the infant during pregnancy. High maternal consumption of milk products during pregnancy may protect children from developing CMA, especially in offspring of non-allergic mothers.

Effect of the prenatal maternal environments and diets on cord blood interleukin-4 and interferon -gamma: A pilot study.

TThe environment of a pregnant woman can affect not only fetal growth and development, but also diseases in childhood. Neonatal cord blood cytokines are commonly used to evaluate the immune development of neonates. The purpose of this study was to evaluate the effects of the environment and diet during pregnancy on IL-4 and IFN-γ in neonatal cord blood. A total of 111 pregnant women participated in this study from April to November 2010. Allergy history, sensitization assessed by the skin prick test, dietary intake and indoor environment were evaluated. IL-4 and IFN-γ levels were measured in the complete cord blood of neonates using real-time PCR. There were 54 pregnant women with allergic disease. Both IL-4 and IFN-γ levels in neonatal cord blood were higher in samples from allergic mothers than in non-allergic mothers (p<0.05). The indoor environment and nutrient intake were not different between allergic and non-allergic mothers, except regarding carpet use. When the cytokine levels were divided into quartiles, lower folate and vitamin B6 intake was associated with the highest levels of IL-4 in neonatal cord blood (p<0.05), and higher folate and vitamin B6 intake was associated with highest levels of IFN-γ in neonatal cord blood. In this study, a strong association between IL-4 and IFN-γ levels in cord blood and the intake of folate and vitamin B6 was found, which indicates that food intake during pregnancy might have a strong influence on IL-4 and IFN-γ levels in cord blood, to a greater extent than environmental factors.

Induction of Oral Immune Tolerance in Infant Mice via Breastfeeding from Allergic and Non-allergic Mothers

Induction of Oral Immune Tolerance in Infant Mice via Breastfeeding from Allergic and Non-allergic Mothers

Association between healthy eating in pregnancy and allergic status of the offspring in childhood

During the past few decades there has been a steady increase in the prevalence of noncommunicable diseases, including allergic disease. Changing lifestyle and subsequent diet may explain this increase seen in the prevalence of atopic disease. Epidemiologic evidence also suggests that diet may be key in the prevention of allergic disease. [1] There are 3 important characteristics in terms of the maternal diet that have been investigated for the prevention of allergic disease: (1) the role of particular nutrients, such as vitamins (A, D, and E), zinc, and fatty acids; (2) the role of particular foods, such as fruits and vegetables and fish; and (3) the total dietary intake, such as a Mediterranean diet or a healthy diet. Research using the healthy eating index tool, specific to the pregnancy diet, found no association between overall healthy eating score and recurrent wheeze in infants at the age of 3 years. [2] However, maternal intake of celery and citrus fruit specifically has been associated with an increased risk of sensitization to food allergens in 2-year-olds. [3] One case-control study found no effect of consumption of fish, butter, and margarine on the development of atopic sensitization in the offspring of allergic mothers; however, a protective effect of fish intake (2–3 times a week or more) was identified in the nonallergic mothers' group with the risk of food sensitization in the offspring reduced by greater than a third. [4] Thus, the question is whether the associations seen are due to the individual nutrients or foods or whether it is part of an overall nutritional composition of the weaning diet. In this study, we aimed to investigate whether maternal diet, specifically seafood intake during pregnancy, is associated with the infant's allergic outcomes in a well-characterized birth cohort with allergy at 3 and 10 years of age.

Breast milk fatty acid composition has a long-term effect on the risk of asthma, eczema, and sensitization.

Levels of n-3 polyunsaturated fatty acids (PUFAs) and n-6 PUFAs in breast milk are associated with the development of allergic diseases up to school age. However, it is unknown whether this relationship persists when the child becomes older. We therefore studied the association between levels of n-3 PUFAs and n-6 PUFAs in breast milk of allergic- and nonallergic mothers and asthma, eczema and sensitization up to the age of 14 years. The study was nested in the ongoing PIAMA birth cohort. At the child's age of 3 months, 276 mothers provided a breast milk sample. Asthma (N total = 269) and eczema (N total = 274) were self-reported up to the child's age of 14 years. Specific serum IgE levels were measured at the ages of 4, 8 and 12 years (N total = 216). Generalized estimating equations analyses were used to take account of repeated observations. Asthma up to the age of 14 years is less prevalent in children of allergic mothers receiving breast milk with higher levels of n-3 long chain polyunsaturated (LCP) fatty acids (OR 0.50; 95% CI 0.31-0.79), and more prevalent in children of nonallergic mothers receiving breast milk with higher levels of n-6LCP (OR 1.86; 95% CI 1.14-3.03). Weaker associations in similar direction were observed for eczema and sensitization. Direction of associations were consistent and of similar magnitude throughout childhood. The association between breast milk fatty acid composition and asthma, eczema and sensitization persists up to the age of 14 years in children of both allergic and nonallergic mothers.

Role of Maternal Allergy on Immune Markers in Colostrum and Secretory Immunoglobulin A in Stools of Breastfed Infants.

Although protection against infectious diseases has been observed among breastfed infants as compared to formula-fed infants, possible benefits of breastfeeding by allergic mothers for allergy prevention remain controversial. The aims of this study were to determine whether maternal allergy would influence immune markers (secretory immunoglobulin A [sIgA], interleukin-8 [IL-8], soluble CD14 [sCD14]) in colostrum and the associations between maternal allergy and fecal sIgA levels in breastfed infants. Study subjects were enrolled from the Prediction of Allergies in Taiwanese Children (PATCH) birth cohort study. Colostrum samples were obtained from 98 lactating mothers. Stool samples were collected from 108 infants within 5 days after birth and at 2 and 4 months of age. We compared concentrations of sIgA, IL-8, and sCD14 in colostrum between mothers with and without a history of allergic disease and allergic sensitization. We also compared fecal sIgA levels between breastfed and formula-fed infants and between infants with allergic and nonallergic mothers. The sIgA concentrations were significantly higher in colostrum from allergic mothers than from nonallergic mothers (P = .01) and from allergic mothers who were immunoglobulin E (IgE) sensitized compared to nonallergic mothers who were not IgE sensitized (P = .023). Breastfed infants had significantly higher fecal sIgA levels as compared to formula-fed infants, regardless of whether their lactating mothers had an allergy (P < .05). We found that breastfeeding is associated with increased infants' fecal sIgA levels and may have potential protective effects to the infants during the first 4 months of life, regardless of whether their lactating mothers have allergies.

Difference in the breast milk proteome between allergic and non-allergic mothers.

BackgroundBreastfeeding has been linked to a reduction in the prevalence of allergy and asthma. However, studies on this relationship vary in outcome, which may partly be related to differences in breast milk composition. In particular breast milk composition may differ between allergic and non-allergic mothers. Important components that may be involved are breast milk proteins, as these are known to regulate immune development in the newborn. The objective of this study was therefore to explore differences in the proteins of breast milk from 20 allergic and non-allergic mothers. The results from this comparison may then be used to generate hypotheses on proteins associated with allergy in their offspring.MethodsMilk samples from allergic and non-allergic mothers were obtained from the PIAMA project, a prospective birth cohort study on incidence, risk factors, and prevention of asthma and inhalant allergy. Non-targeted proteomics technology, based on liquid chromatography and mass spectrometry, was used to compare breast milk from allergic and non-allergic mothers.ResultsNineteen proteins, out of a total of 364 proteins identified in both groups, differed significantly in concentration between the breast milk of allergic and non-allergic mothers. Protease inhibitors and apolipoproteins were present in much higher concentrations in breast milk of allergic than non-allergic mothers. These proteins have been suggested to be linked to allergy and asthma.ConclusionsThe non-targeted milk proteomic analysis employed has provided new targets for future studies on the relation between breast milk composition and allergy.

Transmission of allergen-specific IgG and IgE from maternal blood into breast milk visualized with microarray technology

Transmission of allergen-specific IgG and IgE from maternal blood into breast milk visualized with microarray technology

Imbalance between Th1 and Th2 cells in cord blood is influenced by maternal allergic rhinitis and associated with atopic dermatitis during the first two years of life

To investigate the influence of maternal atopy on cord blood effector T cells and to identify these biologic markers as predictors of atopic dermatitis (AD). Seventy mother-infant pairs were recruited in this prospective birth cohort study. Suspected factors for allergy, including maternal allergic history, total serum IgE, and maternal age at birth, were collected. Mother peripheral blood samples and cord blood were obtained and assayed for the percentage of interferon-γ (IFN-γ) and interleukin 4 (IL-4) producing T cells(Th1 and Th2 respectively) using flow cytometry. Their offspring at the age of 2 years old were evaluated by their dermatologist whether they had AD. Statistical analysis was performed using multiple logistic regression models and receiver-operating characteristic curve was employed to predict atopic dermatitis. Twenty-one allergic and 49 nonallergic mothers were recruited in this study. During the first two years of life, 15.7% children (n = 11) developed a physician-diagnosed AD (all children were the only child in the family). In group with maternal allergic rhinitis, a significantly increased percentage of Th2 was observed in peripheral blood of mother (7.10[1.18;16.1]% vs. 0.37[0.25;0.72]%, U = 10.0, P < 0.05) and cord blood of newborns (1.02[0.57;1.34]% vs. 0.21[0.15;0.42]%, U = 127.5, P < 0.05), respectively. Maternal atopic history did not affect the percentage of Th1 cells in cord blood (0.69[0.40;1.12]% vs.0.50[0.31;0.66]%, U = 361.0, P > 0.05). Children with reduced Th1/Th2 ratio in cord blood had a higher risk to develop AD (OR = 1.72, P = 0.001) . The model including Th1/Th2, maternal allergy, maternal age at birth and maternal total IgE showed high ability to discriminate children with and without AD. AUC was 0.907 (95% CI: 0.804-1.011, P < 0.001). Elevated IL-4⁺CD4⁺ T cells in cord blood were of relevance with maternal allergic history. Imbalance between Th1 cell and Th2 cell at birth are associated with maternal allergy and promoted subsequent AD development.

Prospective Study of Peripregnancy Consumption of Peanuts or Tree Nuts by Mothers and the Risk of Peanut or Tree Nut Allergy in Their Offspring

The etiology of the increasing childhood prevalence of peanut or tree nut (P/TN) allergy is unknown. To examine the association between peripregnancy consumption of P/TN by mothers and the risk of P/TN allergy in their offspring. Prospective cohort study. The 10,907 participants in the Growing Up Today Study 2, born between January 1, 1990, and December 31, 1994, are the offspring of women who previously reported their diet during, or shortly before or after, their pregnancy with this child as part of the ongoing Nurses' Health Study II. In 2006, the offspring reported physician-diagnosed food allergy. Mothers were asked to confirm the diagnosis and to provide available medical records and allergy test results. Two board-certified pediatricians, including a board-certified allergist/immunologist, independently reviewed each potential case and assigned a confirmation code (eg, likely food allergy) to each case. Unadjusted and multivariable logistic regression analyses were used to evaluate associations between peripregnancy consumption of P/TN by mothers and incident P/TN allergy in their offspring. Peripregnancy consumption of P/TN. Physician-diagnosed P/TN allergy in offspring. Among 8205 children, we identified 308 cases of food allergy (any food), including 140 cases of P/TN allergy. The incidence of P/TN allergy in the offspring was significantly lower among children of the 8059 nonallergic mothers who consumed more P/TN in their peripregnancy diet (≥ 5 times vs <1 time per month: odds ratio = 0.31; 95% CI, 0.13-0.75; P(trend) = .004). By contrast, a nonsignificant positive association was observed between maternal peripregnancy P/TN consumption and risk of P/TN allergy in the offspring of 146 P/TN-allergic mothers (P(trend) = .12). The interaction between maternal peripregnancy P/TN consumption and maternal P/TN allergy status was statistically significant (P(interaction) = .004). Among mothers without P/TN allergy, higher peripregnancy consumption of P/TN was associated with lower risk of P/TN allergy in their offspring. Our study supports the hypothesis that early allergen exposure increases tolerance and lowers risk of childhood food allergy.

Maternal allergy is associated with surface‐boundIgEon cord blood basophils

BackgroundThe cell type(s) mediating the maternal influence on allergic disease in children remain unclear. We set out to define the relationship between maternal allergy and frequencies of cord blood (CB) basophils, and plasmacytoid dendritic cells (pDCs); to characterize surface-bound IgE and FcεRI expressions on these cells; and to investigate the association between maternal and CB serum IgE levels with surface-bound IgE and FcεRI expressions.MethodsOne hundred and three mother/infant dyads were recruited prenatally, and maternal allergic history was recorded. Maternal blood was collected prior to delivery, and CB was collected after birth. Flow cytometry was used to identify CB basophils and pDCs and to determine surface-bound IgE and FcεRI expressions.ResultsFrequencies of CB basophils and pDCs were low and not related to maternal history of allergy. Percentages of CB basophils with surface-bound IgE were significantly higher in infants of allergic mothers compared with infants of non-allergic mothers (median, 59.60% vs. 19.70%, p = 0.01). IgE on CB basophils correlated with CB IgE levels (r = 0.72, p < 0.0001), but not with maternal IgE levels (r = 0.26, p = 0.06). IgE on CB pDCs was low and not significantly associated with maternal or CB IgE levels. Similarly, FcεRI expression by CB basophils and pDCs was not significantly associated with maternal or CB IgE levels.ConclusionsFrequencies of CB basophils and pDCs are not influenced by maternal allergy. CB basophils and pDCs have surface-bound IgE and express FcεRI; however, only IgE on CB basophils appears influenced by maternal allergy.