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Maheshwar Bhasin, PhD Student, Centre for Immunology and breastfeeding
Head, Immunology and Breastfeeding
First-of-its-kind findings show that newborns exclusively fed colostrum in their first 72 hours of life were five times less likely to develop a peanut allergy by 12-18 months, and 11 times less likely to develop multiple food allergies (such as egg or cow’s milk) compared with infants who also received formula
Valerie Verhasselt MD, PhD Head, Immunology and Breastfeeding 0402997617 Valerie.verhasselt@thekids.org.au Head, Immunology and Breastfeeding @
Valerie Verhasselt MD, PhD Head, Immunology and Breastfeeding 0402997617 Valerie.verhasselt@thekids.org.au Head, Immunology and Breastfeeding @
Food allergy affects families' quality of life, can be lifelong and life-threatening, urging the identification of early modifiable risk factors. Formula feeding in the first days of life may increase the risk of cow's milk allergy, a risk often attributed to cow's milk allergens exposure. Early formula feeding also reduces the colostrum intake, the first 3 days' milk, which is rich in bioactive compounds critical for immune and gut health. This study investigates whether partial colostrum feeding increases the risk of food allergy beyond cow's milk.
Water chlorination is essential for controlling harmful microbes in drinking water; however, the antimicrobial effects of chlorine-based disinfectants present in tap water may influence early-life gut microbial ecology.
Protection of newborns from infection can be achieved through maternal or vaccine-induced antibodies, but the factors influencing vaccine protection (correlate of protection) and subsequent infant immunity remain insufficiently understood. Further investigation is essential to optimize early-life vaccination strategies.
Previous research has shown that immune development during the first week of life, i.e. ontogeny, is progressive, consistent and robust, involving large numbers of differentially expressed genes at each sampled time point.
Type 1 interferons (T1IFNs) are typically expressed in low concentrations under homeostatic conditions, but upon pathogenic insult or perturbation of the pathway, these critical immune signaling molecules can become either protectors from or drivers of pathology. While essential for initiating antiviral defense and modulating inflammation, dysregulation of T1IFN signaling can contribute to immunopathology, making it and its associated pathways prime targets for immune evasion and disruption by pathogens.