Increased levels of interleukin-8 in BAL fluid from smokers susceptible to pulmonary emphysema

M. Tanino, Tomoko Betsuyaku, K. Takeyabu, Y. Tanino, E. Yamaguchi, K. Miyamoto, M. Nishimura

研究成果: Article

118 引用 (Scopus)

抄録

Background: It has previously been shown that smokers with computed tomographic (CT) evidence of subclinical emphysema have signs of neutrophil activation, despite having no appreciable increase in the number of neutrophils in their bronchoalveolar lavage (BAL) fluid. Methods: The levels of the following chemoattractants in BAL fluid from 61 community based older volunteers classified into four groups according to current smoking status and the presence or absence of emphysema were determined: interleukin 8 (IL-8), epithelial neutrophil activating protein 78 (ENA-78) and leukotriene B4 (LTB4) which are primarily chemotactic for neutrophils; monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1α(MIP-1α) which are predominantly chemotactic for mononuclear leucocytes. Results: Of the five chemoattractants studied, only the level of IL-8 in BAL fluid clearly distinguished between subjects with and without emphysema among current smokers (median values 34.7 and 12.2 pg/ml, respectively, p<0.01). In addition, the levels of IL-8 and neutrophil elastase-α protease inhibitor complex in BAL fluid were significantly correlated (r=0.65, p<0.01). There was no difference in either the release of IL-8 from cultured alveolar macrophages at 24 hours or the expression of IL-8 messenger RNA of alveolar macrophages in the two groups of current smokers with and without emphysema. Conclusion: An accelerated response of IL-8 to chronic smoking is a factor that characterises those smokers who are susceptible to pulmonary emphysema, although the cellular source of IL-8 remains to be determined.

元の言語English
ページ(範囲)405-411
ページ数7
ジャーナルThorax
57
発行部数5
DOI
出版物ステータスPublished - 2002
外部発表Yes

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Pulmonary Emphysema
Bronchoalveolar Lavage Fluid
Interleukin-8
Emphysema
Neutrophils
Chemotactic Factors
Alveolar Macrophages
Secretory Proteinase Inhibitory Proteins
Smoking
Macrophage Inflammatory Proteins
Mononuclear Leukocytes
Neutrophil Activation
Leukotriene B4
Chemokine CCL2
Protease Inhibitors
Volunteers
Messenger RNA

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

これを引用

Tanino, M., Betsuyaku, T., Takeyabu, K., Tanino, Y., Yamaguchi, E., Miyamoto, K., & Nishimura, M. (2002). Increased levels of interleukin-8 in BAL fluid from smokers susceptible to pulmonary emphysema. Thorax, 57(5), 405-411. https://doi.org/10.1136/thorax.57.5.405

Increased levels of interleukin-8 in BAL fluid from smokers susceptible to pulmonary emphysema. / Tanino, M.; Betsuyaku, Tomoko; Takeyabu, K.; Tanino, Y.; Yamaguchi, E.; Miyamoto, K.; Nishimura, M.

:: Thorax, 巻 57, 番号 5, 2002, p. 405-411.

研究成果: Article

Tanino, M, Betsuyaku, T, Takeyabu, K, Tanino, Y, Yamaguchi, E, Miyamoto, K & Nishimura, M 2002, 'Increased levels of interleukin-8 in BAL fluid from smokers susceptible to pulmonary emphysema', Thorax, 巻. 57, 番号 5, pp. 405-411. https://doi.org/10.1136/thorax.57.5.405
Tanino M, Betsuyaku T, Takeyabu K, Tanino Y, Yamaguchi E, Miyamoto K その他. Increased levels of interleukin-8 in BAL fluid from smokers susceptible to pulmonary emphysema. Thorax. 2002;57(5):405-411. https://doi.org/10.1136/thorax.57.5.405
Tanino, M. ; Betsuyaku, Tomoko ; Takeyabu, K. ; Tanino, Y. ; Yamaguchi, E. ; Miyamoto, K. ; Nishimura, M. / Increased levels of interleukin-8 in BAL fluid from smokers susceptible to pulmonary emphysema. :: Thorax. 2002 ; 巻 57, 番号 5. pp. 405-411.
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abstract = "Background: It has previously been shown that smokers with computed tomographic (CT) evidence of subclinical emphysema have signs of neutrophil activation, despite having no appreciable increase in the number of neutrophils in their bronchoalveolar lavage (BAL) fluid. Methods: The levels of the following chemoattractants in BAL fluid from 61 community based older volunteers classified into four groups according to current smoking status and the presence or absence of emphysema were determined: interleukin 8 (IL-8), epithelial neutrophil activating protein 78 (ENA-78) and leukotriene B4 (LTB4) which are primarily chemotactic for neutrophils; monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1α(MIP-1α) which are predominantly chemotactic for mononuclear leucocytes. Results: Of the five chemoattractants studied, only the level of IL-8 in BAL fluid clearly distinguished between subjects with and without emphysema among current smokers (median values 34.7 and 12.2 pg/ml, respectively, p<0.01). In addition, the levels of IL-8 and neutrophil elastase-α protease inhibitor complex in BAL fluid were significantly correlated (r=0.65, p<0.01). There was no difference in either the release of IL-8 from cultured alveolar macrophages at 24 hours or the expression of IL-8 messenger RNA of alveolar macrophages in the two groups of current smokers with and without emphysema. Conclusion: An accelerated response of IL-8 to chronic smoking is a factor that characterises those smokers who are susceptible to pulmonary emphysema, although the cellular source of IL-8 remains to be determined.",
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AU - Betsuyaku, Tomoko

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AU - Yamaguchi, E.

AU - Miyamoto, K.

AU - Nishimura, M.

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AB - Background: It has previously been shown that smokers with computed tomographic (CT) evidence of subclinical emphysema have signs of neutrophil activation, despite having no appreciable increase in the number of neutrophils in their bronchoalveolar lavage (BAL) fluid. Methods: The levels of the following chemoattractants in BAL fluid from 61 community based older volunteers classified into four groups according to current smoking status and the presence or absence of emphysema were determined: interleukin 8 (IL-8), epithelial neutrophil activating protein 78 (ENA-78) and leukotriene B4 (LTB4) which are primarily chemotactic for neutrophils; monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1α(MIP-1α) which are predominantly chemotactic for mononuclear leucocytes. Results: Of the five chemoattractants studied, only the level of IL-8 in BAL fluid clearly distinguished between subjects with and without emphysema among current smokers (median values 34.7 and 12.2 pg/ml, respectively, p<0.01). In addition, the levels of IL-8 and neutrophil elastase-α protease inhibitor complex in BAL fluid were significantly correlated (r=0.65, p<0.01). There was no difference in either the release of IL-8 from cultured alveolar macrophages at 24 hours or the expression of IL-8 messenger RNA of alveolar macrophages in the two groups of current smokers with and without emphysema. Conclusion: An accelerated response of IL-8 to chronic smoking is a factor that characterises those smokers who are susceptible to pulmonary emphysema, although the cellular source of IL-8 remains to be determined.

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