Maternal Allergy Research Articles

Dendritic cell-specific deletion of PKCδ in offspring of allergic mothers prevents the predisposition for development of allergic lung inflammation in offspring.

In humans and in mice, maternal allergy predisposes offspring to development of allergy. In murine models, increased levels of maternal β-glucosylceramides are both necessary and sufficient for the development of allergic predisposition in offspring. Furthermore, increased numbers of CD11b+ dendritic cell subsets in the offspring of allergic mothers are associated with allergic predisposition. In vitro, β-glucosylceramides increase CD11b+ dendritic cell subset numbers through increased PKCδ signaling but it is not known if enhanced PKCδ signaling in dendritic cells is required in vivo. We demonstrate that dendritic cell-specific deletion of PKCδ prevents the β-glucosylceramide-induced increase in CD11b+ dendritic cell subset numbers both in vitro as well as in vivo in the fetal liver of offspring of mothers injected with β-glucosylceramides. Furthermore, dendritic cell-specific deletion of PKCδ in offspring prevents the maternal allergy-induced increase in CD11b+ dendritic cell subsets and decreases allergen-induced IL-5 and eosinophilia in lungs of offspring. However, loss of PKCδ in dendritic cells did not prevent development of allergen-specific IgE. Our study provides mechanistic insight into the function of PKCδ in the origins of allergic disease beginning in utero as well as the development of postnatal allergic lung inflammation.

Associations of air pollution exposures in preconception and pregnancy with birth outcomes and infant neurocognitive development: analysis of the Complex Lipids in Mothers and Babies (CLIMB) prospective cohort in Chongqing, China

ObjectivesTo investigate the associations of traffic-related air pollution exposures in early pregnancy with birth outcomes and infant neurocognitive development.DesignCohort study.SettingEligible women attended six visits in the maternity clinics of two...

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.

Plasma polyamines during pregnancy and their relationships with maternal allergies and the immune response of the neonates

AbstractBackgroundSome studies have reported that polyamine levels may influence immune system programming. The aim of this study was to evaluate the polyamine profile during gestation and its associations with maternal allergy and cytokine production in cord blood cells in response to different allergenic stimuli.MethodsPolyamines were determined in plasma of pregnant women (24 weeks, N = 674) and in umbilical cord samples (N = 353 vein and N = 160 artery) from the Mediterranean NELA birth cohort. Immune cell populations were quantified, and the production of cytokines in response to different allergic and mitogenic stimuli was assessed in cord blood.ResultsSpermidine and spermine were the most prevalent polyamines in maternal, cord venous, and cord arterial plasma. Maternal allergies, especially allergic conjunctivitis, were associated with lower spermine in umbilical cord vein. Higher levels of polyamines were associated with higher lymphocyte number but lower Th2‐related cells in cord venous blood. Those subjects with higher levels of circulating polyamines in cord showed lower production of inflammatory cytokines, especially IFN‐α, and lower production of Th2‐related cytokines, mainly IL‐4 and IL‐5. The effects of polyamines on Th1‐related cytokines production were uncertain.ConclusionsSpermidine and spermine are the predominant polyamines in plasma of pregnant women at mid‐pregnancy and also in umbilical cord. Maternal allergic diseases like allergic conjunctivitis are related to lower levels of polyamines in cord vein, which could influence the immune response of the newborn. Cord polyamine content is related to a decreased Th2 response and inflammatory cytokines production, which might be important to reduce an allergenic phenotype in the neonate.

Short-chain fatty acids (SCFA) in infants’ plasma and corresponding mother’s milk and plasma in relation to subsequent sensitisation and atopic disease

Short-chain fatty acids (SCFAs) in intestinal contents may influence immune function, while less is known about SCFAs in blood plasma. The aims were to investigate the relation between infants' and maternal plasma SCFAs, as well as SCFAs in mother's milk, and relate SCFA concentrations in infant plasma to subsequent sensitisation and atopic disease. Infant plasma (N=148) and corresponding mother's milk and plasma were collected four months postpartum. Nine SCFA (formic, acetic, propionic, isobutyric, butyric, succinic, valeric, isovaleric, and caproic acid) were analysed by UPLC-MS. At 12 months of age, atopic disease was diagnosed by a pediatric allergologist, and sensitisation was measured by skin prick test. All families participated in the Swedish birth cohort NICE (Nutritional impact on Immunological maturation during Childhood in relation to the Environment). Infants with sensitisation, atopic eczema, or food allergy had significantly lower concentrations of five, three, and two SCFAs, respectively, in plasma at four months. Logistic regressions models showed significant negative associations between formic, succinic, and caproic acid and sensitisation [ORadj (95% CI) per SD: 0.41 (0.19-0.91); 0.19 (0.05-0.75); 0.25 (0.09-0.66)], and between acetic acid and atopic eczema [0.42 (0.18-0.95)], after adjusting for maternal allergy. Infants' and maternal plasma SCFA concentrations correlated strongly, while milk SCFA concentrations were unrelated to both. Butyric and caproic acid concentrations were enriched around 100-fold, and iso-butyric and valeric acid around 3-5-fold in mother's milk, while other SCFAs were less prevalent in milk than in plasma. Butyric and caproic acid might be actively transported into breast milk to meet the needs of the infant, although mechanistic studies are needed to confirm this. The negative associations between certain SCFAs on sensitisation and atopic disease adds to prior evidence regarding their immunoregulatory potential. Swedish Research Council (Nr. 2013-3145, 2019-0137 and 2023-02217 to A-S.S.), Swedish Research Councilfor Health, Working Life and Welfare FORTE, Nr 2018-00485 to A.W.), The Swedish Asthma and Allergy Association's Research Fund (2020-0020 to A.S.).

Exploring the epigenetic landscape: The role of 5-hydroxymethylcytosine in neurodevelopmental disorders.

Recent advances in genetic and epigenetic research have underscored the significance of 5-hydroxymethylcytosine (5hmC) in neurodevelopmental disorders (NDDs), such as autism spectrum disorder (ASD) and intellectual disability (ID), revealing its potential as both a biomarker for early detection and a target for novel therapeutic strategies. This review article provides a comprehensive analysis of the role of 5hmC in NDDs by examining both animal models and human studies. By examining mouse models, studies have demonstrated that prenatal environmental challenges, such as maternal infection and food allergies, lead to significant epigenetic alterations in 5hmC levels, which were associated with NDDs in offspring, impacting social behavior, cognitive abilities and increasing ASD-like symptoms. In human studies, researchers have linked alterations in 5hmC levels NDDs through studies in individuals with ASD, fragile X syndrome, TET3 deficiency and ID, specifically identifying significant epigenetic modifications in genes such as GAD1, RELN, FMR1 and EN-2, suggesting that dysregulation of 5hmC played a critical role in the pathogenesis of these disorders and highlighted the potential for targeted therapeutic interventions. Moreover, we explore the implications of these findings for the development of epigenetic therapies aimed at modulating 5hmC levels. The review concludes with a discussion on future directions for research in this field, such as machine learning, emphasizing the need for further studies to elucidate the complex mechanisms underlying NDDs and to translate these findings into clinical practice. This paper not only advances our understanding of the epigenetic landscape of NDDs but also opens up new avenues for diagnosis and treatment, offering hope for individuals affected by these conditions.

Maternal penicillin allergy and infant outcomes: Results from a large administrative cohort

Maternal penicillin allergy and infant outcomes: Results from a large administrative cohort

Study of Allergy and Sensitization Relationship in Children and Parents in Southern China

Introduction: The incidence of allergic diseases has increased globally, with genetics playing an essential role in these conditions’ development. However, there is still a gap in understanding of how parental allergy status affects children’s allergies. Methods: An electronic questionnaire was used to assess allergy-related symptoms in kindergarten children and their parents, with a clinical diagnosis and concurrent serum allergen-specific immunoglobulin E (IgE), total IgE, and blood cell counts obtained. Results: 88 family groups were enrolled, with allergy prevalence of 85.2% in children, 50% in fathers, and 42% in mothers. Allergic rhinoconjunctivitis was the most common allergic disease. When the mother had an allergy, the children’s allergy diagnosis rate was 91.3%; 86.67% when the father had an allergy; and 85.71% when both parents had allergies. The child sensitization rate was 78.26% when the father had sensitization, 59.09% just as the mother had sensitization, and 84.21% when both parents had sensitization. Paternal allergies affected children’s quality of life due to allergic rhinitis but not their rhinitis symptoms. Maternal allergies or sensitization did not significantly affect children’s symptoms or quality-of-life scores. Conclusion: The study found a positive correlation between childhood and parental allergies, and further studies are needed to confirm the findings.

Maternal antibiotic exposure and childhood allergies: The Japan Environment and Children's Study.

The association of maternal antibiotic exposure during pregnancy with childhood allergic diseases remains unclear. We aimed to evaluate the association of maternal exposure to antibiotic use during pregnancy with childhood allergic diseases up to the age of 3 years by using data from a large Japanese birth cohort. We analyzed data on 78,678 pregnant women and their offspring aged 0 to 3 years. Prenatal antibiotic exposure was defined as the use of any antimicrobial agent during pregnancy. Information was collected from maternal interviews and medical record transcripts. The outcome variables in this study included preschool asthma, wheezing, food allergy, atopic dermatitis, eczema, allergic rhinoconjunctivitis, and any allergic disease. We used logistic regression analysis to evaluate the association of antibiotic exposure during pregnancy with childhood allergic diseases. Among the participating mothers, 28.5% used antibiotics during pregnancy. Antibiotic exposure during pregnancy was associated with preschool asthma (adjusted odds ratio [aOR]= 1.12 [95% CI= 1.06-1.19]), wheezing (aOR= 1.11 [95% CI= 1.07-1.15]), allergic rhinoconjunctivitis (aOR= 1.10 [95% CI= 1.03-1.17]) and any allergic disease (aOR= 1.09 [95% CI= 1.05-1.14]) in offspring up to age 3 years. In contrast, maternal antibiotic use was not associated with food allergies, atopic dermatitis, or eczema. Additionally, the significant associations were not influenced by the timing of antibiotic exposure, sex of the infants, or maternal history of allergies. Maternal antibiotic exposure during pregnancy is associated with an increased risk of childhood respiratory allergies.

A novel LC-MS/MS method to characterize the antimicrobial lipid glycerol monolaurate in global human milk

Glycerol monolaurate (GML), a monoglyceride found in human milk (HM), has antimicrobial properties against a broad spectrum of bacteria, viruses, and fungi. In this study, an LC-MS/MS method was developed and validated for quantifying GML in HM based on quantification of two distinct isomers, 1-monolaurin and 2-monolaurin. The method validation included assessments of selectivity (no interferences), linearity (r2 range of 0.9954– 0.9985 and 96 of 98 individual points having residual <15%), accuracy (average recovery of 96.4% across both isomers and a range of spiked levels), and precision (total GML repeatability 6.6% RSD and intermediate precision 9.7% RSD). This validated method was used to measure the concentration of GML in unpasteurized HM from 60 mothers and compared geographical locations (Cincinnati and Shanghai), lactation time (weeks 2 and 26), and self-reported maternal allergy status (yes or no). Our findings suggest GML concentration in unpasteurized HM is considerably lower than previously reported in a study characterizing pasteurized HM. The data reported here highlights a novel, validated method used to quantify GML in HM and identified no differences in total GML concentrations when comparing HM from different geographical locations, lactation times, and mother’s allergy status.

Prenatal allergic inflammation in rats confers sex-specific alterations to oxytocin and vasopressin innervation in social brain regions

Prenatal exposure to inflammation via maternal infection, allergy, or autoimmunity increases one's risk for developing neurodevelopmental and psychiatric disorders. Many of these disorders are associated with altered social behavior, yet the mechanisms underlying inflammation-induced social impairment remain unknown. We previously found that a rat model of acute allergic maternal immune activation (MIA) produced deficits like those found in MIA-linked disorders, including impairments in juvenile social play behavior. The neuropeptides oxytocin (OT) and arginine vasopressin (AVP) regulate social behavior, including juvenile social play, across mammalian species. OT and AVP are also implicated in neuropsychiatric disorders characterized by social impairment, making them good candidate regulators of social deficits after MIA.We profiled how acute prenatal exposure to allergic MIA changed OT and AVP innervation in several brain regions important for social behavior in juvenile male and female rat offspring. We also assessed whether MIA altered additional behavioral phenotypes related to sociality and anxiety. We found that allergic MIA increased OT and AVP fiber immunoreactivity in the medial amygdala and had sex-specific effects in the nucleus accumbens, bed nucleus of the stria terminalis, and lateral hypothalamic area. We also found that MIA reduced ultrasonic vocalizations in neonates and increased the stereotypical nature of self-grooming behavior. Overall, these findings suggest that there may be sex-specific mechanisms underlying MIA-induced behavioral impairment and underscore OT and AVP as ideal candidates for future mechanistic studies.

MicroRNA-322 overexpression reduces neural tube defects in diabetic pregnancies

Hyperglycemia from pregestational diabetes mellitus induces neural tube defects in the developing fetus. Folate supplementation is the only effective way to prevent neural tube defects; however, some cases of neural tube defects are resistant to folate. Excess folate has been linked to higher maternal cancer risk and infant allergy. Therefore, additional interventions are needed. Understanding the mechanisms underlying maternal diabetes mellitus-induced neural tube defects can identify potential targets for preventing such defects. Despite not yet being in clinical use, growing evidence suggests that microRNAs are important intermediates in embryonic development and can serve as both biomarkers and drug targets for disease intervention. Our previous studies showed that maternal diabetes mellitus invivo activates the inositol-requiring transmembrane kinase/endoribonuclease 1α (IRE1α) in the developing embryo and that a high glucose condition invitro reduces microRNA-322 (miR-322) levels. IRE1α is an RNA endonuclease; however, it is unknown whether IRE1α targets and degrades miR-322 specifically or whether miR-322 degradation leads to neural tube defects via apoptosis. We hypothesize that IRE1α can inhibit miR-322 in maternal diabetes mellitus-induced neural tube defects and that restoring miR-322 expression in developing neuroepithelium ameliorates neural tube defects. This study aimed to identify potential targets for preventing maternal diabetes mellitus-induced neural tube defects and to investigate the roles and relationship of a microRNA and an RNA endonuclease in mouse embryos exposed to maternal diabetes mellitus. To determine whether miR-322 reduction is necessary for neural tube defect formation in pregnancies complicated by diabetes mellitus, male mice carrying a transgene expressing miR-322 were mated with nondiabetic or diabetic wide-type female mice to generate embryos with or without miR-322 overexpression. At embryonic day 8.5 when the neural tube is not yet closed, embryos were harvested for the assessment of 3 miR-322 transcripts (primary, precursor, and mature miR-322), tumor necrosis factor receptor-associated factor 3 (TRAF3), and neuroepithelium cell survival. Neural tube defect incidences were determined in embryonic day 10.5 embryos when the neural tube should be closed if there is no neural tube defect formation. To identify which miR-322 transcript is affected by maternal diabetes mellitus and high glucose conditions, 3 miR-322 transcripts were assessed in embryos from dams with or without diabetes mellitus and in C17.2 mouse neural stem cells treated with different concentrations of glucose and at different time points. To determine whether the endonuclease IRE1α targets miR-322, small interfering RNA knockdown of IRE1α or overexpression of inositol-requiring transmembrane kinase/endoribonuclease 1α by DNA plasmid transfection was used to determine the effect of IRE1α deficiency or overexpression on miR-322 expression. RNA immunoprecipitation was performed to reveal the direct targets of inositol-requiring transmembrane kinase/endoribonuclease 1α. Maternal diabetes mellitus suppressed miR-322 expression in the developing neuroepithelium. Restoring miR-322 expression in the neuroepithelium blocked maternal diabetes mellitus-induced caspase-3 and caspase-8 cleavage and cell apoptosis, leading to a neural tube defect reduction. Reversal of maternal diabetes mellitus-inhibited miR-322 via transgenic overexpression prevented TRAF3 up-regulation in embryos exposed to maternal diabetes mellitus. Activated IRE1α acted as an endonuclease and degraded precursor miR-322, resulting in mature miR-322 reduction. This study supports the crucial role of the IRE1α-microRNA-TRAF3 circuit in the induction of neuroepithelial cell apoptosis and neural tube defect formation in pregnancies complicated by diabetes mellitus and identifies IRE1α and miR-322 as potential targets for preventing maternal diabetes mellitus-induced neural tube defects.

Maternal risk factors for preterm birth in Taiwan, a nationwide population-based cohort study

The rate of preterm birth is increasing globally. It causes significant short-term and long-term health care burdens. A comprehensive recognition of the risk factors related to preterm births is important in the prevention of preterm birth. Our study is to investigate the incidence and maternal risk factors of preterm birth from a nationwide population-based perspective. This is a retrospective cohort study. All live births from 2004 to 2014 in Taiwan enrolled. The main data source was Taiwan's Birth Certificate Application (BCA) database. The BCA database was linked with the National Health Insurance Research Database (NHIRD) to establish any links between information on newborns and maternal underlying disease. A total of 1,385,979 births were included in the analysis. The incidence of preterm birth increased gradually in Taiwan from 8.85% in 2004 to 10.73% in 2014. Maternal age, socioeconomic status, maternal allergy and autoimmune diseases, gynecological diseases, and pregnancy-related complications were significant risk factors for preterm birth. The overall incidence of preterm births has gradually increased in Taiwan. Maternal age, socioeconomic status, certain underlying diseases, and pregnancy-related complications were risk factors for preterm birth.

Maternal Dietary Zinc Intake during Pregnancy and Childhood Allergic Diseases up to Four Years: The Japan Environment and Children's Study.

Maternal dietary zinc intake and childhood allergy have inconsistent relationships. Thus, this study aimed to evaluate the influence of low maternal dietary zinc intake during pregnancy on developing pediatric allergic diseases. This study was designed using the Japan Environment and Children's Study dataset. The model building used data from 74,948 mother-child pairs. Maternal dietary zinc intake was estimated based on the food frequency questionnaire, collecting the intake information of 171 food and beverage items. Fitted logistic regression models and generalized estimating equation models (GEEs) estimated the association between energy-adjusted zinc intake and childhood allergic conditions. The energy-adjusted zinc intake did not affect the risk of developing allergic disorders (wheeze, asthma, atopic dermatitis, rhinitis, and food allergy) in offspring. The GEE model revealed similar insignificant odds ratios. No significant association was found between zinc intake during pregnancy and allergic diseases in offspring in early childhood. Further study remains necessary to examine the association between zinc and allergy with reliable zinc status biomarkers in the body.

Clinical chorioamnionitis: where do we stand now?

Intraamniotic infection is an infection resulting in the inflammation of any combination of the amniotic fluid, the placenta, the fetus itself, the fetal membranes, umbilical cord, or the decidua. In the past, an infection of the amnion and chorion or both was dubbed chorioamnionitis. In 2015, a proposal was made by an expert panel that, instead of clinical chorioamnionitis, the name intrauterine inflammation or infection or both be used, abbreviated as Triple I or simply IAI. However, the abbreviation IAI did not gain popularity, and this article uses the term chorioamnionitis. Chorioamnionitis may arise prior to, during, or following labor. It can present as a chronic, subacute, or acute infection. Its clinical presentation is generally referred to as acute chorioamnionitis. The treatment of chorioamnionitis varies widely across the world due to different bacterial causes and the absence of sufficient evidence to support a specific treatment regimen. There are limited randomized controlled trials that have evaluated the superiority of antibiotic regimens for treating amniotic infections during labor. This lack of evidence-based treatment suggests that the current choice of antibiotics is based on limitations in existing research, rather than absolute science. Chorioamnionitis cannot be cured by antibiotic therapy alone without delivery, and therefore it is necessary to make a decision according to the guidelines for induction of labor or acceleration of delivery. When a diagnosis is suspected or established, it is therefore necessary to apply broad-spectrum antibiotics according to the protocol used by each country, and to continue with them until delivery. A commonly recommended first-line treatment for chorioamnionitis is a simple regimen consisting of amoxicillin or ampicillin and once-daily gentamicin. Available information is not sufficient to indicate the best antimicrobial regimen to treat this obstetric condition. However, the evidence that is currently available suggests that patients with clinical chorioamnionitis, primarily women with a gestational age of 34 weeks or more and those in labor, should receive treatment with this regime. However, antibiotic preferences may vary based on local policy, clinician experience and knowledge, bacterial reasons for the infection, antimicrobial resistance patterns, maternal allergies, and drug availability.

Atopic dermatitis: Correlation of distinct risk factors with age of onset in adulthood compared to childhood.

Atopic dermatitis (AD) has long been regarded as a primarily pediatric disease. However, there is growing evidence for a high rate of adult-onset AD. We aimed to characterize factors associated with adult-onset versus childhood-onset AD and controls. We analyzed cross-sectional data of the CK-CARE-ProRaD cohorts Bonn, Augsburg, Davos, Zürich of 736 adult patients stratified by age of AD onset (childhood-onset <18 years: 76.4% (subsets: 0 to 2; ≥2 to 6; ≥7 to 11; ≥12 to 18); adult-onset ≥18 years: 23.6% (subsets: ≥18 to 40; ≥41 to 60; ≥61) and 167 controls (91 atopic, 76 non-atopic)). We identified active smoking to be associated with adult-onset AD versus controls (adjusted Odds Ratio (aOR) = 5.54 [95% Confidence Interval: 1.06-29.01] vs. controlsnon-atopic , aOR = 4.03 [1.20-13.45] vs. controlsatopic ). Conjunctivitis showed a negative association versus controlsatopic (aOR = 0.36 [0.14-0.91]). Food allergy (aOR = 2.93 [1.44-5.96]), maternal food allergy (aOR = 9.43 [1.10-80.95]), palmar hyperlinearity (aOR = 2.11 [1.05-4.25]), and academic background (aOR = 2.14 [1.00-4.54]) increased the odds of childhood-onset AD versus controlsatopic . Shared AD-associated factors were maternal AD (4-34x), increased IgE (2-20x), atopic stigmata (2-3x) with varying effect sizes depending on AD onset and control group. Patients with adult-compared to childhood-onset had doubled odds of allergic rhinitis (aOR = 2.15 [1.12-4.13]), but reduced odds to feature multiple (3-4) atopic comorbidities (aOR = 0.34 [0.14-0.84]). Adult-onset AD, particularly onset ≥61 years, grouped mainly in clusters with low contributions of personal and familial atopy and high frequencies of physical inactivity, childhood-onset AD, particularly infant-onset, mainly in "high-atopic"-clusters. The identified associated factors suggest partly varying endo- and exogeneous mechanisms underlying adult-onset versus childhood-onset AD. Our findings might contribute to better assessment of the individual risk to develop AD throughout life and encourage prevention by non-smoking and physical activity as modifiable lifestyle factors.

Factors associated with secretory IgA levels in colostrum and breastmilk

Background Secretory IgA (sIgA) content of breastmilk in the first postpartum month is a reflection of the pregnant woman's immune response to environmental antigen exposure. The role of secretory IgA in breastmilk is to protect and support the development of the neonatal immune response in early life.&#x0D; Objective To examine possible factors associated with sIgA levels in breastmilk and colostrum, including environmental exposure, food consumed, maternal history of atopy, and the appearance of allergic symptoms in infants. As a secondary objective, we determined the association between infant factors (IgE, exposure to cigarette smoke) and maternal factors (sIgA, maternal allergies) with infant allergies.&#x0D; Methods This prospective cohort study of 80 postpartum mothers and their infants was conducted at Sultan Agung Islamic Hospital, Semarang. We collected maternal colostrum on the second or third postpartum day and mature milk between the 22nd to 25th postpartum day. Exposure factors to mothers and infants in the final trimester of pregnancy up to one month postpartum was recorded through a questionnaire and home visits. The infant’s IgE level was measured at 4 months of age.&#x0D; Results Mean colostrum sIgA was 108.9 (SD 16.5) mg/dL (95%CI 97.9 to 121.1 mg/dL) and mean mature milk sIgA was 94.1 (SD 23.9) mg/dL (95%CI 89.1 to 99.2 mg/dL). Mean colostrum sIgA levels were higher in mothers exposed to cigarette smoke [119.1 (SD 1.7) vs. 92.9 (SD 1.5) mg/dL; P=0.026] and frequent infections [128.2 (SD 1.7) vs. 95.9 (SD 1.6) mg/dL; P=0.007] compared to that in unexposed mothers. Mean colostrum sIgA was also higher in mothers with atopic allergy than in those without (136.8 mg/dL vs. 99.3 mg/dL; p=0.017) and in mothers of infants with IgE levels &gt;29 IU/ml than in mothers of infants with IgE levels &lt;29 IU/mL (136.8 vs. 101.2 mg/mg/dL; P=0.045). Elevated colostrum sIgA (&gt;136.8 mg/dL) was not associated with allergies in the infants (P=0.269).&#x0D; Conclusions Maternal atopic allergy and frequent infections are associated with increased colostrum sIgA levels. Breastmilk sIgA levels are not associated with allergies in the infant. Maternal exposure to antigens may stimulate the production of specific breastmilk sIgA.

Maternal Penicillin Allergy and Infant Outcomes: Results from a Large, Administrative Cohort

Group B Streptococcus (GBS) is a leading cause of neonatal sepsis. Pregnant women are screened for colonization, and antibiotics are administered during labor to those who test positive to prevent newborn infection. Penicillin or ampicillin are given to women without a penicillin allergy, and cefazolin, clindamycin, or vancomycin are administered to women who report a penicillin allergy. We examined the outcomes of infants born to GBS-positive mothers with and without a reported penicillin allergy.

Risk of asthma in offspring of asthmatic fathers versus mothers: A population-based study of 21,000 individuals in Denmark

Parental asthma or allergy have been linked to higher risk of asthma in a child; this occurs to a variable extent in different study populations. Moreover, it is debated whether maternal more so than paternal asthma history is a stronger predisposing factor: while in some countries/populations the maternal effect was clearly seen over paternal, in others the parental effects were equivalent, and in a few studies paternal effect dominated. Here we aimed to determine parental asthma and allergy effect in the Danish GEneral SUburban population Study (GESUS).This cross-sectional study has involved 21,362 adults aged 20+ years in the suburbs of Copenhagen. We used a combination of questionnaire approach, history of prescribed asthma medications and pulmonary function testing to determine odds ratios for maternal and paternal (and combined) asthma and allergy linked to asthma in the test subjects. We found that the input of maternal vs. paternal asthma effect was approximately equal (age and sex-adjusted OR 2.46, 95% CI: 2.15–2.81 for asthmatic mothers vs. 2.97, 2.58–3.42 for asthmatic fathers), except for the “ever asthma” age and sex-adjusted odds ratios where paternal allergy seems to have conferred a marginally greater effect (age and sex-adj. OR 1.96 for maternal allergy vs. 2.44 for paternal allergy, p = 0.03). Stratifying for gestational tobacco smoking did not affect the maternal results.We conclude that in the GESUS study parental asthma or allergy were strongly linked to higher asthma risk in offspring, without a prominent maternal or paternal effect.

Associative factors for atopic dermatitis and other atopic diseases in middle-aged adults: A population-based birth cohort study among 5373 subjects.

The study aimed to examine parental, longitudinal and current associative factors for atopic dermatitis (AD) and to compare those to other atopic diseases in 46-year-old adults. Questionnaire data from the Northern Finland Birth Cohort 1966 study were used. To analyze allergic sensitization, skin prick tests (n = 5373) were performed for birch, timothy, cat, and house dust mite at age 46. Maternal (odds ratio [OR]1.81; 95% confidence interval [CI]1.25-2.59)and paternal allergy (OR 2.54; CI 1.76-3.64), sensitization to any of the four tested aeroallergens (OR 1.56; CI 1.04-2.30) as well as polysensitization (OR 3.04; CI 2.10-4.37) were associated with current AD. Living on a farm in infancy was negatively associated with allergic rhinitis, allergic conjunctivitis, and atopic multimorbidity. Current AD (OR 2.65; CI 1.44-4.60) and all atopic diseases associated with indoor air related symptoms. Current AD associated with other atopic diseases, most strongly with allergic rhinitis (OR 4.92; CI 3.92-6.22). Current AD in a 46-year-old general population occurred frequently with allergic rhinitis, allergic conjunctivitis, and asthma in the Northern Finland Birth Cohort study 1966. Parental allergy and sensitization to common aeroallergens were found as shared associative factors for AD, allergic rhinitis, allergic conjunctivitis, and asthma. AD and other atopic diseases associated with symptoms related to poor indoor air quality. In daily practice, it is important to take these comorbidities into consideration when treating patients with AD.