Complement C3a and C4a increased in plasma of patients with aspirin-induced asthma

Seung Ha Lee, Tai Youn Rhim, Yun Sung Choi, Ji Won Min, Sung Ho Kim, Sun Young Cho, Young-Ki Paik, Choon Sik Park

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Rationale: Aspirin-induced asthma (AIA) is a distinct clinical syndrome that affects up to 10% of adults with asthma. Although eicosanoid metabolites appear to play an important role in AIA, the exact pathogenic mechanism for the syndrome remains obscure. In addition, the proposed mechanism fails to explain why aspirin does not cause bronchoconstriction in all individuals. Objectives: We aimed to identify proteins that were differentially expressed in between AIA and aspirin-tolerant asthma (ATA) plasma. Methods and Main Results: By using a proteomics approach, six proteins were found to be differentially expressed in plasma between patients with AIA and patients with ATA at baseline, and eight proteins were significantly up- or down-regulated after aspirin challenge in patients with AIA. These proteins, which were identified by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, can be classified into four groups: complement components, apolipoproteins, modified albumin, and unknown proteins. Among them, the complement component levels in plasma were validated by using ELISA. Plasma concentrations of C3a and C4a were higher in patients with AIA (n = 30) than in patients with ATA (n = 24). After the aspirin challenge, C3 decreased in both patients with AIA and those with ATA, but the C3a concentration increased in the AIA patient group (p = 0.019). Moreover, C3a and C4a levels and the ratios of C3a/C3 and C4a/C4 were correlated with the changes of FEV1 values after aspirin challenge. Conclusions: Aspirin intolerance may be related to alterations in the levels of complements, as well as those of lipoprotein and other proteins.

Original languageEnglish
Pages (from-to)370-378
Number of pages9
JournalAmerican Journal of Respiratory and Critical Care Medicine
Volume173
Issue number4
DOIs
Publication statusPublished - 2006 Feb 15

Fingerprint

Complement C4a
Aspirin Induced Asthma
Complement C3a
Aspirin
Asthma
Proteins
Bronchoconstriction
Eicosanoids
Apolipoproteins
Proteomics
Lipoproteins

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine

Cite this

Lee, Seung Ha ; Rhim, Tai Youn ; Choi, Yun Sung ; Min, Ji Won ; Kim, Sung Ho ; Cho, Sun Young ; Paik, Young-Ki ; Park, Choon Sik. / Complement C3a and C4a increased in plasma of patients with aspirin-induced asthma. In: American Journal of Respiratory and Critical Care Medicine. 2006 ; Vol. 173, No. 4. pp. 370-378.
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abstract = "Rationale: Aspirin-induced asthma (AIA) is a distinct clinical syndrome that affects up to 10{\%} of adults with asthma. Although eicosanoid metabolites appear to play an important role in AIA, the exact pathogenic mechanism for the syndrome remains obscure. In addition, the proposed mechanism fails to explain why aspirin does not cause bronchoconstriction in all individuals. Objectives: We aimed to identify proteins that were differentially expressed in between AIA and aspirin-tolerant asthma (ATA) plasma. Methods and Main Results: By using a proteomics approach, six proteins were found to be differentially expressed in plasma between patients with AIA and patients with ATA at baseline, and eight proteins were significantly up- or down-regulated after aspirin challenge in patients with AIA. These proteins, which were identified by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, can be classified into four groups: complement components, apolipoproteins, modified albumin, and unknown proteins. Among them, the complement component levels in plasma were validated by using ELISA. Plasma concentrations of C3a and C4a were higher in patients with AIA (n = 30) than in patients with ATA (n = 24). After the aspirin challenge, C3 decreased in both patients with AIA and those with ATA, but the C3a concentration increased in the AIA patient group (p = 0.019). Moreover, C3a and C4a levels and the ratios of C3a/C3 and C4a/C4 were correlated with the changes of FEV1 values after aspirin challenge. Conclusions: Aspirin intolerance may be related to alterations in the levels of complements, as well as those of lipoprotein and other proteins.",
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Complement C3a and C4a increased in plasma of patients with aspirin-induced asthma. / Lee, Seung Ha; Rhim, Tai Youn; Choi, Yun Sung; Min, Ji Won; Kim, Sung Ho; Cho, Sun Young; Paik, Young-Ki; Park, Choon Sik.

In: American Journal of Respiratory and Critical Care Medicine, Vol. 173, No. 4, 15.02.2006, p. 370-378.

Research output: Contribution to journalArticle

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T1 - Complement C3a and C4a increased in plasma of patients with aspirin-induced asthma

AU - Lee, Seung Ha

AU - Rhim, Tai Youn

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AU - Min, Ji Won

AU - Kim, Sung Ho

AU - Cho, Sun Young

AU - Paik, Young-Ki

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N2 - Rationale: Aspirin-induced asthma (AIA) is a distinct clinical syndrome that affects up to 10% of adults with asthma. Although eicosanoid metabolites appear to play an important role in AIA, the exact pathogenic mechanism for the syndrome remains obscure. In addition, the proposed mechanism fails to explain why aspirin does not cause bronchoconstriction in all individuals. Objectives: We aimed to identify proteins that were differentially expressed in between AIA and aspirin-tolerant asthma (ATA) plasma. Methods and Main Results: By using a proteomics approach, six proteins were found to be differentially expressed in plasma between patients with AIA and patients with ATA at baseline, and eight proteins were significantly up- or down-regulated after aspirin challenge in patients with AIA. These proteins, which were identified by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, can be classified into four groups: complement components, apolipoproteins, modified albumin, and unknown proteins. Among them, the complement component levels in plasma were validated by using ELISA. Plasma concentrations of C3a and C4a were higher in patients with AIA (n = 30) than in patients with ATA (n = 24). After the aspirin challenge, C3 decreased in both patients with AIA and those with ATA, but the C3a concentration increased in the AIA patient group (p = 0.019). Moreover, C3a and C4a levels and the ratios of C3a/C3 and C4a/C4 were correlated with the changes of FEV1 values after aspirin challenge. Conclusions: Aspirin intolerance may be related to alterations in the levels of complements, as well as those of lipoprotein and other proteins.

AB - Rationale: Aspirin-induced asthma (AIA) is a distinct clinical syndrome that affects up to 10% of adults with asthma. Although eicosanoid metabolites appear to play an important role in AIA, the exact pathogenic mechanism for the syndrome remains obscure. In addition, the proposed mechanism fails to explain why aspirin does not cause bronchoconstriction in all individuals. Objectives: We aimed to identify proteins that were differentially expressed in between AIA and aspirin-tolerant asthma (ATA) plasma. Methods and Main Results: By using a proteomics approach, six proteins were found to be differentially expressed in plasma between patients with AIA and patients with ATA at baseline, and eight proteins were significantly up- or down-regulated after aspirin challenge in patients with AIA. These proteins, which were identified by matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, can be classified into four groups: complement components, apolipoproteins, modified albumin, and unknown proteins. Among them, the complement component levels in plasma were validated by using ELISA. Plasma concentrations of C3a and C4a were higher in patients with AIA (n = 30) than in patients with ATA (n = 24). After the aspirin challenge, C3 decreased in both patients with AIA and those with ATA, but the C3a concentration increased in the AIA patient group (p = 0.019). Moreover, C3a and C4a levels and the ratios of C3a/C3 and C4a/C4 were correlated with the changes of FEV1 values after aspirin challenge. Conclusions: Aspirin intolerance may be related to alterations in the levels of complements, as well as those of lipoprotein and other proteins.

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