Effects of histamine on Th1/Th2 cytokine balance

Purpose of review With the disturbing increase in allergic disease, there is a pressing need to determine the causes, pathogenesis and safe avenues for disease prevention. Although events in early life appear important, no causal pathways have been identified. This review examines new developments in the area of foetal and early postnatal immune maturation. It secondly addresses early predisposing influences and protective factors that may have a future role in allergy prevention. Recent findings New developments in the understanding of the ontogeny of allergen-specific immune responses in atopic infants are discussed, including the role of early type 1 and 2 immune responses, and how these are influenced by perinatal antigen presenting cell and T-cell immaturity. The controversial role of early dietary exposures including breastfeeding, food allergens, hydrolyzed formulae and other dietary factors including omega-3 fatty acids are discussed in the context of the most recent literature. Equally contentious, the role of early house dust and pet allergen exposure is discussed in light of new epidemiological studies and disappointing early results of multicentre allergen avoidance studies. Finally, a number of studies in animals and humans suggest that bacterial products can influence early immune development, providing a new potential therapeutic avenue for disease treatment and prevention. Summary Complex multifactorial genetic and environmental interactions make research in this area difficult and apparent associations with allergic disease may not be causal in nature. Many current targets for prevention, such as early allergen exposure and infant feeding practices, are proving to be ineffective and may not be directly implicated in rising rates of disease.

Early origins of allergic disease: a review of processes and influences during early immune development.

Background Although there are recognised associations between psychological and immune function, the effects of maternal depressive symptoms on fetal immune development have not been investigated. Methods This study examined the relationship between maternal depression scores as assessed by the Beck Depression Inventory (BDI) in the second trimester and measure of neonatal immune function measured in cord blood. This study was conducted in a cohort of women ( n  = 83) who had received either fish oil containing 3.7 g/day n -3 polyunsaturated fatty acid ( n -3PUFA) or a placebo from 20 weeks gestation as part of a randomised controlled trial. Results At 20 weeks gestation, prior to the intervention, 22% of women in the study manifested mild to moderate depressive symptoms (BDI ⩾10). Neonates of these women had higher lymphoproliferative responses to a range of stimuli (including egg ovalbumin and cat allergen) compared with neonates of women with normal BDI scores ( n -3/ n -6 PUFA status. Conclusion This exploratory study supports the notion that maternal mood in pregnancy may have the potential to influence fetal immune development. Further studies are needed to determine the significance of this.

Maternal mood scores in mid-pregnancy are related to aspects of neonatal immune function.

Since early prevention is regarded as an important corner stone in the management of atopic diseases, the identification of reliable markers detecting individuals at risk are of major interest. Therefore, many efforts have been made to unravel reliable predictors for atopy which might identify children at risk and allow the initiation of preventive strategies at an early stage. In the past, much scientific energy has been forced in particular on the development of as noninvasive methods as possible to reach this goal. It is obvious that the identification of markers for atopy at the earliest time of life – namely immediately after birth – represents one of the most attractive attempts. In consequence various studies have been initiated to address this issue investigating markers for atopy in cord blood. Most of them have been geared to our current knowledge about cellular and soluble factors which are dysregulated in adolescent atopic individuals. Although the findings of these studies will improve our knowledge about the initial evolution of atopy, several parameters evaluated did not show any association or have led to almost conflicting results. In order to provide an up-date about the current developments in this field, recent research findings on predictive factors for atopy in cord blood are summarized in the following synopsis.

In search for predictive factors for atopy in human cord blood.

The hygiene hypothesis states that childhood asthma develops as a result of decreased exposure to infectious agents during infancy and early childhood. This results in the persistence of the neonatal T helper lymphocyte 2 immunophenotype, thereby predisposing the child to atopic disease. While multiple studies support the hygiene hypothesis in asthma ontogeny, the evidence remains inconclusive; multiple other environmental exposures in early childhood also alter predisposition to asthma. Moreover, the current paradigm for asthma development extends far beyond simple childhood environmental exposures to include fetal development, genetic predisposition, and interactions of the developmental state and genetics with the environment.

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Childhood infections and asthma: at the crossroads of the hygiene and Barker hypotheses.

Background: Despite our knowledge that maternal inheritance influences the development of asthma in childhood, attempts to identify a clear-cut Th2-oriented cytokine production by T

Donatella Bologni

Papers

CD4+IL13+ T lymphocytes at birth and the development of wheezing and/or asthma during the 1st year of life.