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      소아 천식 환아에서 혈청 IL-13 및 eotaxin 농도와기관지과민성의 관계 = Relationship of serum IL-13 and eotaxin level withairway hyperresponsiveness in children with asthma

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      https://www.riss.kr/link?id=A104549121

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      다국어 초록 (Multilingual Abstract)

      Purpose:Asthma is characterized by the presence of airway hyperresponsiveness(AHR) and inflammation. The extensive eosinophil infiltration into the lung is the hallmark of asthma and contributes to the damage of respiratory epithelium during late phase airway responses. Eotaxin is the major eosinophil chemoattractant found in bronchoalveolar lavage(BAL) fluid of allergic inflammation. IL-13 has been known to induce the expression of exotaxin and eosinophilia. IL-13 also induces airway inflammation, mucus production and leads to marked fibrosis, airway remodeling and AHR. We investigated whether serum IL-13 levels can reflect the presence of airway hyperresponsiveness in children with asthma, and the relationship between serum IL-13 and eotaxin levels.
      Methods:Using sandwich enzyme-linked immunosorbent assay, the serum IL-13 and eotaxin levels were measured in 13 atopic asthmatics, 5 atopic non-asthmatics and 12 control subjects. Metacholine challenge tests were performed in all subjects. Airway hyperresponsiveness to metacholine was expressed as provocative concentration of metacholine causing a 20% fall in FEV1[PC20 mg/mL]. PC20 value of 25 mg/mL was used as a cut-off for defining a AHR.
      Results:Serum IL-13 levels showed positive correlation with eotaxin levels. Serum IL-13 and eotaxin levels showed no differences among atopic asthmatics, atopic non-asthmatics and control subjects. And there were no differences serum IL-13 and eotaxin levels in children with and without AHR and atopy. Serum IL-13 and eotaxin levels did not correlate with logPC20 levels.
      Conclusion:IL-13 is closely related to the eotaxin release. But serum IL-13 and eotaxin per se can't predict the severity of airway hyperresponsiveness. IL-13 and eotaxin may have local effect on respiratory epithelium or there can be some factors to induce airway hyperresponsiveness other than serum IL-13 in asthmatic airways.
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      Purpose:Asthma is characterized by the presence of airway hyperresponsiveness(AHR) and inflammation. The extensive eosinophil infiltration into the lung is the hallmark of asthma and contributes to the damage of respiratory epithelium during late pha...

      Purpose:Asthma is characterized by the presence of airway hyperresponsiveness(AHR) and inflammation. The extensive eosinophil infiltration into the lung is the hallmark of asthma and contributes to the damage of respiratory epithelium during late phase airway responses. Eotaxin is the major eosinophil chemoattractant found in bronchoalveolar lavage(BAL) fluid of allergic inflammation. IL-13 has been known to induce the expression of exotaxin and eosinophilia. IL-13 also induces airway inflammation, mucus production and leads to marked fibrosis, airway remodeling and AHR. We investigated whether serum IL-13 levels can reflect the presence of airway hyperresponsiveness in children with asthma, and the relationship between serum IL-13 and eotaxin levels.
      Methods:Using sandwich enzyme-linked immunosorbent assay, the serum IL-13 and eotaxin levels were measured in 13 atopic asthmatics, 5 atopic non-asthmatics and 12 control subjects. Metacholine challenge tests were performed in all subjects. Airway hyperresponsiveness to metacholine was expressed as provocative concentration of metacholine causing a 20% fall in FEV1[PC20 mg/mL]. PC20 value of 25 mg/mL was used as a cut-off for defining a AHR.
      Results:Serum IL-13 levels showed positive correlation with eotaxin levels. Serum IL-13 and eotaxin levels showed no differences among atopic asthmatics, atopic non-asthmatics and control subjects. And there were no differences serum IL-13 and eotaxin levels in children with and without AHR and atopy. Serum IL-13 and eotaxin levels did not correlate with logPC20 levels.
      Conclusion:IL-13 is closely related to the eotaxin release. But serum IL-13 and eotaxin per se can't predict the severity of airway hyperresponsiveness. IL-13 and eotaxin may have local effect on respiratory epithelium or there can be some factors to induce airway hyperresponsiveness other than serum IL-13 in asthmatic airways.

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      국문 초록 (Abstract)

      목 적 : 기관지 천식은 만성적인 기도염증과 기관지과민성을 특징으로 하는 질환이다. 항원으로 유발한 폐조직이나, 기관지세척액에서 호산구 및 여러 염증세포가 관찰되며 eotaxin과 Th2 세포에서 유래한 여러 사이토카인의 증가가 관찰된다. 이 중 IL- 13은 조직 호산구증에 중요한 케모카인인 eotaxin의 발현을 증가시키며, 만성염증, 점액분비증가, 평활근수축 등을 유발하여 기관지과민성을 일으키는 강력한 사이토카인이다. 본 연구는 혈청에서 IL-13 및 eotxin 농도를 측정하여 두 인자간의 상관관계를 알아보고, 기관지과민성 예측을 위한 간접평가방법으로서의 임상적 유용성을 알아보고자 하였다.방 법 : 아토피 천식 환아 13명, 아토피 비천식 환아 5명 그리고 건강한 어린이 13명을 대상으로 하여, 혈청에서 IL-13 및 eotaxin 농도를 측정하고 IL-13과 eotaxin과의 상관관계 및 각 군간 비교를 하였다. 또한 기관지 과민성 및 아토피 유무에 따른 혈청 IL-13, eotaxin 농도를 조사하였다.결 과 : 혈청 IL-13 농도와 eotaxin 농도 사이에는 양의 상관관계가 존재하였다. 아토피 천식군, 아토피 비천식군 및 대조군에서 혈청 IL-13 및 eotaxin 농도 차이는 없었다. 기관지 과민성 및 아토피 여부에 따라 혈청 IL-13 및 eotaxin 농도를 비교하였으나, 이들간에 유의한 차이는 없었다. LogPC20와 혈청 IL- 13, eotaxin 농도간에는 유의한 상관관계가 없었다.
      번역하기

      목 적 : 기관지 천식은 만성적인 기도염증과 기관지과민성을 특징으로 하는 질환이다. 항원으로 유발한 폐조직이나, 기관지세척액에서 호산구 및 여러 염증세포가 관찰되며 eotaxin과 Th2 세포...

      목 적 : 기관지 천식은 만성적인 기도염증과 기관지과민성을 특징으로 하는 질환이다. 항원으로 유발한 폐조직이나, 기관지세척액에서 호산구 및 여러 염증세포가 관찰되며 eotaxin과 Th2 세포에서 유래한 여러 사이토카인의 증가가 관찰된다. 이 중 IL- 13은 조직 호산구증에 중요한 케모카인인 eotaxin의 발현을 증가시키며, 만성염증, 점액분비증가, 평활근수축 등을 유발하여 기관지과민성을 일으키는 강력한 사이토카인이다. 본 연구는 혈청에서 IL-13 및 eotxin 농도를 측정하여 두 인자간의 상관관계를 알아보고, 기관지과민성 예측을 위한 간접평가방법으로서의 임상적 유용성을 알아보고자 하였다.방 법 : 아토피 천식 환아 13명, 아토피 비천식 환아 5명 그리고 건강한 어린이 13명을 대상으로 하여, 혈청에서 IL-13 및 eotaxin 농도를 측정하고 IL-13과 eotaxin과의 상관관계 및 각 군간 비교를 하였다. 또한 기관지 과민성 및 아토피 유무에 따른 혈청 IL-13, eotaxin 농도를 조사하였다.결 과 : 혈청 IL-13 농도와 eotaxin 농도 사이에는 양의 상관관계가 존재하였다. 아토피 천식군, 아토피 비천식군 및 대조군에서 혈청 IL-13 및 eotaxin 농도 차이는 없었다. 기관지 과민성 및 아토피 여부에 따라 혈청 IL-13 및 eotaxin 농도를 비교하였으나, 이들간에 유의한 차이는 없었다. LogPC20와 혈청 IL- 13, eotaxin 농도간에는 유의한 상관관계가 없었다.

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      참고문헌 (Reference)

      1 "Upregulation of IL-13 concentraion in vivo the IL-13 variant associated with bronchial asthma" 109 : 980-987, 2002

      2 "The role of IL-13 in established allergic airway disease" 169 : 6482-6489, 2002

      3 "The guideline for diagnosis and management of childhood asthma" Sowha Co 5-87, 1999

      4 "The Th2 lymphocyte products IL-4 and IL-13 rapidly induce airway hyperresponsiveness through direct effects on resident airway cells" 26 : 202-208, 2002

      5 "Standardization of bronchial inhalation challenge procedures" 56 : 323-58, 1975

      6 "Relationship between airway hyperresposiveness and duration of asthma in children" 23 : 77-83, 2003

      7 "Pulmonary expression of interleukin-13 causes inflmmation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production" 103 : 779-789, 1999

      8 "Localized eosinophil degranulation mediates disease in tropical pulmonary eosinophilia" 71 : 1337-1342, 2003

      9 "Interleukin-13 upregulates eotaxin expression in airway epithelial cells by a STAT6-dependent mechanism" 24 : 755-761, 2001

      10 "Inter leukin-13:Central mediator of allergic asthma" 282 : 2258-2261, 1998

      1 "Upregulation of IL-13 concentraion in vivo the IL-13 variant associated with bronchial asthma" 109 : 980-987, 2002

      2 "The role of IL-13 in established allergic airway disease" 169 : 6482-6489, 2002

      3 "The guideline for diagnosis and management of childhood asthma" Sowha Co 5-87, 1999

      4 "The Th2 lymphocyte products IL-4 and IL-13 rapidly induce airway hyperresponsiveness through direct effects on resident airway cells" 26 : 202-208, 2002

      5 "Standardization of bronchial inhalation challenge procedures" 56 : 323-58, 1975

      6 "Relationship between airway hyperresposiveness and duration of asthma in children" 23 : 77-83, 2003

      7 "Pulmonary expression of interleukin-13 causes inflmmation, mucus hypersecretion, subepithelial fibrosis, physiologic abnormalities, and eotaxin production" 103 : 779-789, 1999

      8 "Localized eosinophil degranulation mediates disease in tropical pulmonary eosinophilia" 71 : 1337-1342, 2003

      9 "Interleukin-13 upregulates eotaxin expression in airway epithelial cells by a STAT6-dependent mechanism" 24 : 755-761, 2001

      10 "Inter leukin-13:Central mediator of allergic asthma" 282 : 2258-2261, 1998

      11 "IL-13 induces eosinophil recruitment into the lung by an IL-5 and eotaxin dependent mechanism" 108 : 594-601, 2001

      12 "IL-13 and IL-4 cause eotaxin release in human airway smooth muscle cells:a role for ERK" 282 : 847-852, 2002

      13 "Haplotype structure and evidence for positive selection at the human IL13 locus" 21 : 29-35, 2004

      14 "Haemopoietic mechanisms in murine allergic upper and lower airway inflammation" 114 : 386-396, 2005

      15 "Evaluation of inflammation in childhood asthma" 44 : 334-339, 2001

      16 "Eotaxin-2 and IL-5 cooperate in the lung to regulate IL-13 production and airway eosinophilia and hyperreactivity" 112 : 935-943, 2003

      17 "Eosinophils express functional IL-13, in eosinophilic inflammatory disease" 169 : 1021-1027, 2002

      18 "Effect of Th2 cytokines on chemokine expression in the lung:IL-13 potently induces eotaxin expression by airway epithelial cells" 162 : 2477-2487, 1999

      19 "Crucial factors for bronchial hyperresponsiveness in children with mild asthma" 15 : 142-149, 2005

      20 "Critical role for IL-13 in the development of allergen-induced airway hyperreactivity" 167 : 4668-4675, 2001

      21 "Comparison of plasma eotaxin family level in aspirin- induced and aspirin-tolerant asthma patient" 128 : 127-132, 2005

      22 "Chemokines in asthma:Cooperative interaction between chemokines and IL-13" 111 : 227-242, 2003

      23 "Association between an interleukin-13 promotor polymorphism and atopy" 30 : 355-359, 2003

      24 "Anti-IL-13 monoclonal antibody inhibits airway hyperresponsiveness, inflammation and airway remodeling" 28 : 224-232, 2004

      25 "A 10 year follow-up childhood asthma:Potential risk factors on persistence of nonspecific bronchial hyperresponsiveness" 12 : 82-92, 2002

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