Am. J. Respir. Crit. Care Med., Vol 153, No. 6, Jun 1996, 1785-1789.
Development of bronchial hyperreactivity following transient absence of salivary IgA
M Gleeson, RL Clancy, MJ Hensley, AW Cripps, RL Henry, JH Wlodarczyk and PG Gibson
Hunter Immunology Unit, Hunter Area Pathology Service, Royal Newcastle Hospital, Newcastle, Australia.
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.
