Epicutaneous sensitization: role in food allergy and response to immune deviation

• Main Authors: Kuang-Yang Hsieh, 謝光煬
• Other Authors: Rong-Hwa Lin
• Format: Others
• Language: en_US
• Published: 2003
• Online Access: http://ndltd.ncl.edu.tw/handle/93988629842162110106

博士 === 國立臺灣大學 === 免疫學研究所 === 91 === Exposure to common allergens through the skin is likely, but not well known, to be a natural route of sensitization for various allergic diseases. In this study, we attempted to clarify whether epicutaneous (EC) exposure to protein antigen can induce food allergy. In mice epicutaneously pre-sensitized to ovalbumin (OVA), subsequent oral challenge with OVA induced systemic anaphylaxis-like symptoms, with elevated plasma histamine levels as well as histologic changes in intestine and lung. These results identify a novel role of EC sensitization in the pathogenesis of food allergy. In the presence of anti-IL-4 antibodies, EC sensitization still induced a Th2-predominant cellular food-allergic response in lungs. In contrast, intraperitoneal (IP) sensitization induced a Th1-predominant response in the absence of IL-4. These results suggest that EC and IP sensitization may differ in the mechanism for Th2 induction and may respond differently to immune deviation. Using oral administration of FIP-fve, a fungal immunomodulatory protein isolated from the edible mushroom Flammulina velutipes, we established a protocol of prophylactic immune deviation and examined its effect on food-allergic responses induced by IP or EC sensitization. Mice receiving oral FIP-fve during IP sensitization to OVA had an impaired OVA-specific IgE response with a Th1-predomonant cytokine profile. These mice were protected from systemic anaphylaxis-like symptoms induced by subsequent oral challenge with OVA. In contrast, oral administration of FIP-fve during EC sensitization to OVA failed to inhibit the specific IgE response and food-allergic responses induced by subsequent oral challenge. The relative role of EC sensitization in various allergic diseases deserves further exploration. The poor response of EC sensitization to systemic immune deviation is worth to note with respect to the treatment of allergic diseases. Further investigation on the molecular mechanisms of EC sensitization will certainly contribute to the fight against allergic diseases.