Adenoids are known as immunosecretory organs and those in atopic children present cellular and cytokine profiles different from those of non-atopic children. We hypothesized that locally produced total IgE and allergen-specific antibodies could be involved in the inflammatory responses in adenoid tissue. Local productions of total IgE and Dermatophagoides pteronyssinus (DP)-specific IgE, IgA, IgG1, and IgG4 antibodies were evaluated, as well as their relationships with the markers of allergic inflammation within adenoid tissue. Eighteen atopic subjects, who were sensitized to more than one common aeroallergen, and 22 non-atopic subjects undergoing adenotonsillectomy, were recruited. Immunoassays using adenoid tissue homogenate were performed to quantify the levels of total IgE, eosinophil cationic protein (ECP), and mast cell tryptase. DP-specific IgE, IgA, IgG1, and IgG4 antibodies, soluble IL-2 receptors (sIL-2R), soluble CD23 (sCD23), and IL-6 were measured by ELISA. All parameters measured in adenoid tissue homogenate were presented as a ratio to the albumin level found in the adenoid. Median level of total IgE in adenoid tissue homogenate was significantly higher in atopic individuals than in non-atopic individuals. Median values of DP-specific IgE and IgA antibodies were significantly higher in atopics than in non-atopics (p = 0.001, p = 0.006, respectively), while no differences were seen in DP-specific IgG1 and IgG4 antibodies. ECP and sCD23 levels in adenoid homogenate were significantly higher in atopics than in non-atopics (p = 0.026, p = 0.048, respectively), while no significant differences were noted in tryptase, sIL-2R, and IL-6 levels. The levels of DP-specific IgE, IgA, IgG1, and IgG4 antibodies in adenoid homogenate correlated significantly with ECP levels, but not with those of sIL-2R, sCD23, and IL-6. The presence of total IgE and DP-specific antibodies in adenoid tissue was confirmed to be more prominent in atopics. In conclusion, locally-produced total IgE and DP-specific antibodies may contribute to eosinophilic inflammation in adenoid tissue in atopic children.