알레르기 행진: 아토피피부염에서 천식으로의 이행
Allergic March: Progression from Atopic Dermatitis to Asthma
2
조회
0
다운로드
9
인용
0
참고문헌
키워드
초록
Allergic march is progression of allergic disorders from atopic dermatitis in infancy to asthma or allergic rhinitis later. Most prospective epidemiologic studies suggest that early atopic dermatitis is a risk factor for the development of asthma, whereas only some subtypes of early atopic dermatitis with concomitant wheeze or less prevalent sensitization were recently reported to be at increased risk of development of asthma during childhood. There is a question as to whether atopic dermatitis itself is a true risk factor for the development of asthma later or allergic march just reflects the order of appearance of atopic dermatitis and asthma or allergic rhinitis. Filaggrin gene mutations are associated with atopic dermatitis as well as asthma with atopic dermatitis in the Western countries, and skin barrier dysfunction can initiate systemic sensitization in the mouse model. Therefore, skin barrier dysfunction can explain partly the mechanism of allergic march. Thymic stromal lymphopoietin and interleukin-17 can also be involved in the development of asthma in the mouse model of allergic march. Moreover, microbial organisms on the skin can enhance or modulate the immunologic mechanism of allergic march. A few pharmacologic agents have been investigated to interrupt allergic march, and the results are not promising. To find effective interruption of allergic march, a well-defined target, further understanding of the mechanism, and development of novel agents or combination of previous agents to modulate immune response remain to be solved.
Abstract
Allergic march is progression of allergic disorders from atopic dermatitis in infancy to asthma or allergic rhinitis later. Most prospective epidemiologic studies suggest that early atopic dermatitis is a risk factor for the development of asthma, whereas only some subtypes of early atopic dermatitis with concomitant wheeze or less prevalent sensitization were recently reported to be at increased risk of development of asthma during childhood. There is a question as to whether atopic dermatitis itself is a true risk factor for the development of asthma later or allergic march just reflects the order of appearance of atopic dermatitis and asthma or allergic rhinitis. Filaggrin gene mutations are associated with atopic dermatitis as well as asthma with atopic dermatitis in the Western countries, and skin barrier dysfunction can initiate systemic sensitization in the mouse model. Therefore, skin barrier dysfunction can explain partly the mechanism of allergic march. Thymic stromal lymphopoietin and interleukin-17 can also be involved in the development of asthma in the mouse model of allergic march. Moreover, microbial organisms on the skin can enhance or modulate the immunologic mechanism of allergic march. A few pharmacologic agents have been investigated to interrupt allergic march, and the results are not promising. To find effective interruption of allergic march, a well-defined target, further understanding of the mechanism, and development of novel agents or combination of previous agents to modulate immune response remain to be solved.
참고문헌 (31)
- Zheng T, "The atopic march: progression from atopic dermatitis to allergic rhinitis and asthma", Allergy Asthma Immunol Res, 3, pp.67~73 (2011)
- Martinez FD, "Asthma and wheezing in the first six years of life. The Group Health Medical Associates", N Engl J Med, 332, pp.133~138 (1995)
- Klinnert MD, "Onset and persistence of childhood asthma: predictors from infancy", Pediatrics, 108, pp.E69~ (2001)
- Arshad SH, "Early life risk factors for current wheeze, asthma, and bronchial hyperresponsiveness at 10 years of age", Chest, 127, pp.502~508 (2005)
- Illi S, "Multicenter Allergy Study Group. The natural course of atopic dermatitis from birth to age 7 years and the association with asthma", J Allergy Clin Immunol, 113, pp.925~931 (2004)
- Lowe AJ, "Do boys do the atopic march while girls dawdle?", J Allergy Clin Immunol, 121, pp.1190~1195 (2008)
- Almqvist C, "Early predictors for developing allergic disease and asthma: examining separate steps in the 'allergic march'", Clin Exp Allergy, 37, pp.1296~1302 (2007)
- Burgess JA, "Childhood eczema and asthma incidence and persistence: a cohort study from childhood to middle age", J Allergy Clin Immunol, 122, pp.280~285 (2008)
- Lowe AJ, "The temporal sequence of allergic sensitization and onset of infantile eczema", Clin Exp Allergy, 37, pp.536~542 (2007)
- Herrick CA, "Th2 responses induced by epicutaneous or inhalational protein exposure are differentially dependent on IL-4", J Clin Invest, 105, pp.765~775 (2000)
- He R, "Epicutaneous antigen exposure induces a Th17 response that drives airway inflammation after inhalation challenge", Proc Natl Acad Sci U S A, 104, pp.15817~15822 (2007)
- Spergel JM, "Epicutaneous sensitization with protein antigen induces localized allergic dermatitis and hyperresponsiveness to methacholine after single exposure to aerosolized antigen in mice", J Clin Invest, 101, pp.1614~1622 (1998)
- Soumelis V, "Human epithelial cells trigger dendritic cell mediated allergic inflammation by producing TSLP", Nat Immunol, 3, pp.673~680 (2002)
- Zhang Z, "Thymic stromal lymphopoietin overproduced by keratinocytes in mouse skin aggravates experimental asthma", Proc Natl Acad Sci U S A, 106, pp.1536~1541 (2009)
- Cork MJ, "New perspectives on epidermal barrier dysfunction in atopic dermatitis: gene-environment interactions", J Allergy Clin Immunol, 118, pp.3~21 (2006)
- Seidenari S, "Objective assessment of the skin of children affected by atopic dermatitis: a study of pH, capacitance and TEWL in eczematous and clinically uninvolved skin", Acta Derm Venereol, 75, pp.429~433 (1995)
- Spergel JM, "From atopic dermatitis to asthma : the atopic march", Ann Allergy Asthma Immunol, 105, pp.99~106 (2010)
- Palmer CN, "Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis", Nat Genet, 38, pp.441~446 (2006)
- Smith FJ, "Loss-of-function mutations in the gene encoding filaggrin cause ichthyosis vulgaris", Nat Genet, 38, pp.337~342 (2006)
- Fallon PG, "A homozygous frameshift mutation in the mouse Flg gene facilitates enhanced percutaneous allergen priming", Nat Genet, 41, pp.602~608 (2009)
- Henderson J, "The burden of disease associated with filaggrin mutations: a population-based, longitudinal birth cohort study", J Allergy Clin Immunol, 121, pp.872~877 (2008)
- Lee DE, "Association between filaggrin mutations and atopic dermatitis in Korean pregnant women", Int J Dermatol (2011)
- Leyden JJ, "Staphylococcus aureus in the lesions of atopic dermatitis", Br J Dermatol, 90, pp.525~530 (1974)
- Breuer K, "Bacterial infections and atopic dermatitis", Allergy, 56, pp.1034~1041 (2001)
- Bunikowski R, "Evidence for a disease-promoting effect of Staphylococcus aureus-derived exotoxins in atopic dermatitis", J Allergy Clin Immunol, 105, pp.814~819 (2000)
- Leung DY, "The role of superantigens in human diseases: therapeutic implications for the treatment of skin diseases", Br J Dermatol, 139(53), pp.17~29 (1998)
- Bright JJ, "Superantigens augment antigen-specific Th1 responses by inducing IL-12 production in macrophages", J Leukoc Biol, 65, pp.665~670 (1999)
- Mandron M, "Human dendritic cells conditioned with Staphylococcus aureus enterotoxin B promote TH2 cell polarization", J Allergy Clin Immunol, 117, pp.1141~1147 (2006)
- Yu J, "Epicutaneous exposure to Staphylococcal superantigen enterotoxin B enhances allergic lung inflammation via an IL-17A dependent mechanism", PLoS One, 7, pp.e39032~ (2012)
- Warner JO, "A double-blinded, randomized, placebo-controlled trial of cetirizine in preventing the onset of asthma in children with atopic dermatitis: 18 months' treatment and 18 months' posttreatment follow-up", J Allergy Clin Immunol, 108, pp.929~937 (2001)
- Simons FE, "Safety of levocetirizine treatment in young atopic children: An 18-month study", Pediatr Allergy Immunol, 18, pp.535~542 (2007)