Past, present, and future of allergy in Korea

Abstract

Korean allergology has made great progress in keeping pace with global scientific advances in spite of a short history. Outstanding academic and scientific researches have been performed in a variety of allergy fields in Korea. Epidemiologic studies revealed increasing prevalence of asthma and allergic diseases and considerable morbidity and mortality in Korea. Novel inhalant allergens such as citrus red mite and two-spotted spider mite as causes of asthma and allergic rhinitis have been discovered and reported in Korea. Bidirectional translational researches have been performed and are underway to elucidate the pathogenesis of asthma and allergy, mechanisms of airway inflammation and remodeling, and new therapeutic modalities for asthma and allergic diseases. Experimental asthma models of different phenotypes according to exposed levels of lipopolysaccharide or double-stranded RNA suggested the crucial role of the innate immunity in the development of allergic airway inflammation and a new insight for asthma pathogenesis, in which both Th1 and Th2 inflammation are involved. In the field of genetic researches, numerous genetic associations with asthma and asthma-related phenotypes, such as atopy, IgE production, and airway hyperresponsiveness, have been demonstrated in Korean population. The Easy Asthma Management (EAM) program, a computer-assisted asthma management program, is anticipated to facilitate the achievement of more successful clinical outcomes by filling the gaps between guidelines and actual practices. The Integration of these multi-disciplinary allergy research resources and translation of scientific achievements to the bedside and society will lead to better allergy and asthma control in Korea.

Keywords: Allergy; Korea; asthma.

Fig. 1

Brief view of Korean allergology history. (A) The first general meeting of KAAACI (Foundation meeting: 30 November, 1972). (B) The first Korean allergy congress (8 December, 1973). (C) Professor Seok-Young Kang and early members of the first Allergy Clinic in Korea. (D) (D1) The First Edition of "Allergy" (The Journal of The Korean Society of Allergology) issued in June, 1981. (D2) The name of the journal changed to "Journal of Asthma, Allergy and Clinical Immunology" in 1998. (D3) The first edition of Asthma, Allergy & Immunologic Research (AAIR), the international journal of KAAA CI and KAPARD in January, 2010. E. The 5th West-Pacific Allergy Symposium (WAPS) and the 7th Korea-Japan Joint Allergy Symposium which was concurrently held with the 25th Anniversary Congress of KAAACI (June, 1997, Seoul). (F) Organizing committee members of The 5th Asian Pacific Congress of Allergology and Clinical Immunology (APCACI) and the 7th WPAS (October, 2002, Seoul). (G) The first general meeting of the Korea Asthma Allergy Foundation (KAF) (October, 2003). (H) The second Global Alliance of Chronic Respiratory Diseases (GARD) general meeting and GARD Korea launching in Seoul, Korea (May 2004).

Fig. 2

Growth of Korean allergy SCI papers. These data were obtained from a PubMed search (keyword [allergy or asthma or hypersensitivity] and affiliation [Korea])

Fig. 3

Prevalence of asthma and allergic diseases based on epidemiologic studies in Korea. (A) Changes in the prevalence of asthma symptoms in Korean school-aged children between 1995 and 2000. (B) Prevalence of current asthma according to age in Korean adults. (C) Prevalence of perennial allergic rhinitis, (C1) changes in prevalence between 1991 and 2001, (C2) prevalence according to age. (D) Prevalence of atopic dermatitis and food allergies based on questionnaires in Korean school-aged children.

Fig. 4

Outdoor spider mites as novel allergens that cause asthma and allergic rhinitis as shown on the cover papers of international allergy journals.

Fig. 5

Mortality rate and leading causes of death in Korea: changes between 1992 and 2007.

Fig. 6

Both Th1 and Th2 inflammation are involved in asthma pathogenesis. (A) Different asthma phenotypes according to the co-exposed dose of LPS with allergen. (B) Th2 airway inflammation induced by low-dose ds-RNA co-exposure with allergen. (C) Th1 airway inflammation induced by high-dose ds-RNA coexposure with allergen.