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Background: The maternal and infant microbiome may influence infant cardiovascular risk through immune programming. The maternal vagino-enteric microbiome is often sampled for group B streptococcus (GBS) colonization during pregnancy. Our aim was to investigate the association between maternal GBS colonization, intrapartum antibiotics, antenatal pet exposure and infant aortic intima-media thickness (aIMT), an intermediate vascular phenotype, and whether this association varied by mode of delivery.Methods: The Barwon Infant Study is a population-derived pre-birth cohort. Perinatal data were collected on participants. Women were tested for vagino-enteric group B streptococcus (GBS) colonization during third trimester. Six-week infant aIMT was measured by trans-abdominal ultrasound. Adjustment for confounders included maternal age, pre-pregnancy body mass index (BMI), smoking, socioeconomic status, gestational diabetes, length of gestation, infant sex, birthweight and aortic internal diameter.Results: Data were available on 835 mother-infant pairs. Of these, 574 (69%) women delivered vaginally; of those, 129 (22%) were GBS-colonized; and of these women, 111 (86%) received prophylactic intrapartum antibiotics. An association between maternal GBS colonization and infant aIMT was observed among those delivered vaginally (β = 19.5 µm, 95% CI 9.5, 29.4; P  < 0.0001) but not by Caesarean section ( P for interaction = 0.02). A similar pattern was seen for intrapartum antibiotics. There was a negative association between antenatal pet exposure and aIMT observed in those delivered vaginally.Conclusion: Maternal GBS colonization and intrapartum antibiotics were associated with increased infant aIMT in those delivered vaginally, whereas antenatal pet exposure was associated with decreased aIMT. These data suggest that differences in early life microbial experience may contribute to an increased cardiovascular risk. [ABSTRACT FROM AUTHOR]

The modern environment is associated with an increasing burden of non-communicable diseases (NCDs). Mounting evidence implicates environmental exposures, experienced early in life (including in utero), in the aetiology of many NCDs, though the cellular/molecular mechanism(s) underlying this elevated risk across the life course remain unclear. Epigenetic variation has emerged as a candidate mediator of such effects. The Barwon Infant Study (BIS) is a population-derived birth cohort study (n = 1074 infants) with antenatal recruitment, conducted in the south-east of Australia (Victoria). BIS has been designed to facilitate a detailed mechanistic investigation of development within an epidemiological framework. The broad objectives are to investigate the role of specific environmental factors, gut microbiota and epigenetic variation in early-life development, and subsequent immune, allergic, cardiovascular, respiratory and neurodevelopmental outcomes. Participants have been reviewed at birth and at 1, 6, 9 and 12 months, with 2- and 4-year reviews under way. Biological samples and measures include: maternal blood, faeces and urine during pregnancy; infant urine, faeces and blood at regular intervals during the first 4 years; lung function at 1 month and 4 years; cardiovascular assessment at 1 month and 4 years; skin-prick allergy testing and food challenge at 1 year; and neurodevelopmental assessment at 9 months, 2 and 4 years. Data access enquiries can be made at [www.barwoninfantstudy.org.au] or via [peter.vuillermin@deakin.edu.au]. [ABSTRACT FROM AUTHOR]

HealthNuts is a single-centre, multi-wave, population-based longitudinal study designed to assess prevalence, determinants, natural history and burden of allergy (particularly food allergy) in the early years of life. It is novel in the use of serial food challenge measures within its population frame to confirm food allergy. The cohort comprises 5276 children initially recruited at age 12 months from council-run immunization sessions across Melbourne, Australia. As well as parent-completed questionnaires and researcher-observed eczema status, all infants underwent skin-prick testing to egg, peanut, sesame and either cow's milk or shellfish, and those with detectable wheals underwent food challenges to determine clinical allergy. In wave 2, conducted at age 4 years, validated questionnaires collected data on asthma, allergic rhinitis (hay fever), eczema and food allergies. Food challenges were repeated in children previously identified as food allergic to determine resolution. In wave 3, all children (irrespective of food allergy status) were invited for clinical assessment at age 6 years, including lung function, physical measurements, skin-prick testing to foods and aeroallergens and food challenges if food sensitized. Biological specimens (blood, cheek swabs) were collected at each wave for ancillary immunological, genetic and epigenetic studies. Applications to access data and/or samples can be submitted to [katrina.allen@mcri.edu.au]. [ABSTRACT FROM AUTHOR]