Production of salivary immunoglobulin A and suppression of Dermatophagoides pteronyssinus-induced airway inflammation by local nasal immunotherapy.
BACKGROUND
Local nasal immunotherapy (LNIT) is an effective immunotherapeutic modality, especially when targeting a single immunodominant peptide from an allergen. However, the working mechanisms of LNIT are poorly understood. We hypothesized that LNIT with a mixture of group 2 allergens of Dermatophagoides pteronyssinus (Der p 2) protein and fungal immunomodulatory peptide (FIP) would generate suppression of Der p-induced airway inflammation through immunoglobulin (Ig) A secretion in the airways.


METHODS
Mice were sensitized with recombinant Der p 2 (rDer p 2) and Der p followed by LNIT with rDer p 2 in conjunction with FIP. After intratracheal challenge with rDer p 2 and Der p, the airway inflammation was determined by analyzing the cell subpopulation and cytokine concentration in the bronchoalveolar lavage fluid. The allergen-specific IgE, IgG2a and IgG in the sera and IgA in the saliva were measured by ELISA.


RESULTS
LNIT with rDer p 2 in conjunction with FIP could downregulate the lymphocyte infiltration in both rDer p 2- and Der p-induced airway inflammation. Both total and specific IgA in the saliva were increased after LNIT. Serum levels of IL-4, IL-10 and specific IgE were reduced and the specific IgG2a and IgG increased after LNIT. After LNIT, there was a reduction of airway hypersensitivity at 30 min after allergen challenge in the rDer p 2-and Der p-sensitized mice, with a significant decrease only in rDer p 2-sensitized mice.


CONCLUSIONS
LNIT with rDer p 2 in conjunction with FIP was not only able to suppress rDer p 2-induced airway inflammation but also generate suppression of Der p-induced airway inflammation. The simultaneous reduction of IL-4 and IL-10 indicated that IL-10-producing cells were not activated by LNIT. The increment of IgA in the airway might play a role in the prevention of airway inflammation.
Liu
Yi-Hsia
YH
Section of Allergy and Immunology, Taichung Veterans General Hospital, Taichung, Taiwan, ROC.
Tsai
Jaw-Ji
JJ
D000281:Administration, Intranasal; D000818:Animals; D039741:Antigens, Dermatophagoides / Q000008:administration & dosage / Q000276:immunology / Q000627:therapeutic use*; D060829:Arthropod Proteins; D040002:Dermatophagoides pteronyssinus / Q000276:immunology; D003888:Desensitization, Immunologic / Q000379:methods*; D005260:Female; D005656:Fungal Proteins / Q000008:administration & dosage / Q000276:immunology / Q000627:therapeutic use*; D007071:Immunoglobulin A, Secretory / Q000096:biosynthesis* / Q000276:immunology; D037102:Lectins / Q000008:administration & dosage / Q000276:immunology / Q000627:therapeutic use*; D008168:Lung / Q000276:immunology / Q000473:pathology; D051379:Mice; D008807:Mice, Inbred BALB C; D011014:Pneumonia / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D012463:Saliva / Q000276:immunology*
D039741:Antigens, Dermatophagoides; D060829:Arthropod Proteins; C451163:Dermatophagoides pteronyssinus antigen p 2; D005656:Fungal Proteins; D007071:Immunoglobulin A, Secretory; D037102:Lectins