This study investigated the result of attending pre-school on mucosal immunity. atopic (< .05). Higher IgG levels were associated with exposure to ETS (< .001), while lower levels were associated to having atopy. Higher IgM levels were associated with previous childcare experience (< .01) whilst having been hospitalised was associated with having low salivary IgM levels (< .01). Lagged analyses demonstrated that immunological parameters were affected by the number of respiratory infections in the preceding 2 months. 1. Introduction The mucosal immune system begins to develop shortly after conception, and whilst structurally complete at birth, it is functionally immature [1]. Functional development is rapidly stimulated after birth by the ingestion and inhalation of bacterial and food antigens and mitogens. The salivary glands have long been recognised as part of the common mucosal immune system [2], and as such, salivary secretions have been often used to assess mucosal immune competence in humans. Numerous studies have looked at the development of the mucosal immune system in the early years of childhood Mouse monoclonal to ER in order to gain some insight into the maturation of the host mucosal defences in children. Whilst some have shown that salivary immunoglobulin levels continue to increase throughout the childhood years [3], others have found that adult levels are reached by seven years [4C8] and even as early as 12 to 18 months of age [9, GW843682X 10]. Although the literature is not GW843682X conclusive on the postnatal ontogeny, what is clear is that the timing and GW843682X pattern of the increase from infant to adult levels appear to depend on environmental influences [11C14]. The development of mucosal immunity is profoundly affected by exposure to infection. The ontogeny patterns for mucosal antibodies in young children appear to reflect the degree of antigenic exposure in their environment. Increased antigenic exposure of infants through poor hygiene and health in developing countries [13, 14] and hospitalisation or daycare attendance in developed countries [9] results in high levels of antibodies in saliva that can occur at an earlier age [13, 14]. Early life events appear to have a critical influence on the ultimate pattern of immune maturation [1], and there has been a pressing need for longitudinal studies to understand how immune responses evolve in children and the impact on long-term clinical outcomes. However, to date, much of the information regarding the impact of environmental stimuli on the developing immune system has been anecdotal. The common interpretation is that older siblings and childcare attendance are indirect measures of early life infections and that early life infections have a preventative effect on the development of atopic disorders [15] and infectious illness. This study was designed to examine several factors that may impact the development of mucosal immunocompetence in young children. Children were studied during their pre-school year as this would be their first encounter with the increased antigenic exposure associated with starting school. Children aged 3.5 to 5 years attending pre-school were monitored for one school year (February to December) to ascertain whether any alteration in mucosal immune function could be linked to environmental, developmental, and clinical events. The effects were monitored using various markers of potential mucosal immune stimuli, such as the number of siblings in the family, days of attendance at daycare facilities, and known modifiers of mucosal immunity such as environmental tobacco smoke (ETS) exposure. A record was kept of the general health status of the children during the year and episodes of gastrointestinal tract (GIT), and respiratory (RT) symptoms were recorded by the parents. Saliva samples were collected at regular intervals throughout the year and were analysed for immunoglobulin levels IgA, IgG, and IgM and = 37). 2.5. Covariates The determinants of interest included gender, atopy, and ETS exposure. Atopy was defined as a history of eczema, asthma, urticaria, and.