Based on the observation that children with a history of atopic disease show significantly increased levels of cleaved secretory lgA in nasopharyngeal secretions, we have previously formulated the hypothesis that bacteria-induced local deficiencies of the immune barrier of the upper respiratory tract may be a contributing factor in the development and perpetuation of atopic diseases. To evaluate this hypothesis, 25 infants were subjected to clinical, bacteriologic, and immunologic examination at the age of 18 mo, 30 mo, and 5 y. The 11 infants, who showed clinical and immunologic evidence of atopic disease at the age of 18 mo, harbored significantly higher proportions of lgA1 protease-producing bacteria (median, 36%; range, 14–64%) than the 14 healthy infants (median, 5%; range, 0.4–14%). No statistically significant differences were observed at the two subsequent examinations, but healthy children showed a statistically significant increase in proportions of lgA1 protease-producing bacteria in the pharynx with increasing age. lgA1 protease-producing bacteria detected includedStreptococcus mitis biovar1.Hoemophilus influenzae, Haemophilus parahaemolyticus, Streptococcus pneumoniae, andNeisseria meningitidis, of which the first mentioned species was mainly responsible for the difference observed at the 18-mo examination. Percentage proportions of lgA1 protease-producing bacteria were significantly related to passive smoking which may stimulate the premature and more pronounced pharyngeal colonization of the atopic infants with the lgA1 protease-producing variant ofS. mitisbiovar 1. The results of the study support the hypothesis that lgA1 protease-producing bacteria colonizing the upper respiratory tract jeopardize the local immune barrier and, thereby, may facilitate the penetration of potential allergens resulting in atopic disease.