title: Development of bronchial hyperreactivity following transient absence of salivary IgA.
abstract: In a birth cohort of 114 normal children, this study examined the hypothesis that a transient absence of salivary IgA in the first year of life was associated with an increased risk of developing atopy, asthma, or bronchial hyperreactivity (BHR) later in life. Episodes of transient absence of IgA in saliva, of less than 1 mo, occurred in 18% of the study population in the first year of life. The children were assessed at age 7.5 to 12 yr for the presence of atopy (skin prick test to inhaled allergens), asthma (wheeze in the previous 12 mo), and BHR (histamine provocation). The transient absence of salivary IgA in the first year of life was associated with an increased risk of BHR (adjusted odds ratio [Adj OR]: 11.6; 95% confidence interval [CI]: 2.2 to 60.9) and a trend toward a lowered risk of atopy to inhaled allergens (raw OR: 0.35; CI: 0.11 to 1.11). There was no relationship between the transient absence of salivary IgA and a clinical diagnosis of asthma (Adj OR: 0.9; CI: 0.2 to 3.6). The inconsistency in the relationships between the transient absence of salivary IgA and atopy, asthma, and BHR supports the concept that atopy, wheeze, and bronchial hyperreactivity are independent clinical outcomes. One possible explanation for the relationships observed in this study is that the transient absence of IgA in saliva in the first year of life identifies a cohort with mucosal hypoimmunity. These subjects are thus less likely to develop atopy and less able to effectively respond to a mucosal infection. Presentation of a mucosal antigen in these subjects may subsequently be associated with an inappropriate inflammatory response, which conditions bronchial hyperreactivity, and which is independent of atopy.
authors.affiliation: Hunter Immunology Unit, Hunter Area Pathology Service, Royal Newcastle Hospital, Newcastle, Australia.
authors.forename: M
authors.initials: M
authors.lastname: Gleeson
authors.forename: R L
authors.initials: RL
authors.lastname: Clancy
authors.forename: M J
authors.initials: MJ
authors.lastname: Hensley
authors.forename: A W
authors.initials: AW
authors.lastname: Cripps
authors.forename: R L
authors.initials: RL
authors.lastname: Henry
authors.forename: J H
authors.initials: JH
authors.lastname: Wlodarczyk
authors.forename: P G
authors.initials: PG
authors.lastname: Gibson
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects; D001249:Asthma / Q000209:etiology / Q000276:immunology*; D016535:Bronchial Hyperreactivity / Q000209:etiology / Q000276:immunology*; D002648:Child; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000209:etiology / Q000276:immunology*; D007070:Immunoglobulin A / Q000378:metabolism*; D007223:Infant; D008297:Male; D016017:Odds Ratio; D011446:Prospective Studies; D012129:Respiratory Function Tests; D012135:Respiratory Sounds / Q000276:immunology; D012306:Risk; D012463:Saliva / Q000276:immunology*; D012882:Skin Tests
chemical_list: D000393:Air Pollutants; D007070:Immunoglobulin A