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Statins enhance the anti-inflammatory effects of inhaled corticosteroids in asthmatic patients through increased induction of indoleamine 2, 3-dioxygenase

Background We have previously shown that inhaled corticosteroids activate indoleamine 2, 3-dioxygenase (IDO) activity through increased IL-10 secretion. Statins might enhance the anti-inflammatory effects of corticosteroids. Objective In a double-blind study we added simvastatin to patients with mil... Full description

Journal Title: Journal of allergy and clinical immunology 2010, Vol.126 (4), p.754-762.e1
Main Author: Maneechotesuwan, Kittipong, MD, PhD
Other Authors: Ekjiratrakul, Wuttichai, MD , Kasetsinsombat, Kanda, MSc , Wongkajornsilp, Adisak, MD, PhD , Barnes, Peter J., DSc, FRS
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Alma/SFX Local Collection
Publisher: New York, NY: Mosby, Inc
ID: ISSN: 0091-6749
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title: Statins enhance the anti-inflammatory effects of inhaled corticosteroids in asthmatic patients through increased induction of indoleamine 2, 3-dioxygenase
format: Article
creator:
  • Maneechotesuwan, Kittipong, MD, PhD
  • Ekjiratrakul, Wuttichai, MD
  • Kasetsinsombat, Kanda, MSc
  • Wongkajornsilp, Adisak, MD, PhD
  • Barnes, Peter J., DSc, FRS
subjects:
  • Abridged Index Medicus
  • Adult
  • Allergy and Immunology
  • Anti-Inflammatory Agents - administration & dosage
  • Anti-Inflammatory Agents - therapeutic use
  • Anti-inflammatory drugs
  • Antiasthmatic agents
  • Antitubercular agents
  • Asthma
  • Asthma - drug therapy
  • Biological and medical sciences
  • Budesonide - administration & dosage
  • Budesonide - therapeutic use
  • Cellular biology
  • Cholesterol
  • Chronic obstructive pulmonary disease, asthma
  • Corticosteroids
  • Cytokines
  • Double-Blind Method
  • Drug Synergism
  • Drug Therapy, Combination
  • Enzyme Induction
  • Enzymes
  • Female
  • Fundamental and applied biological sciences. Psychology
  • Fundamental immunology
  • Humans
  • Immunopathology
  • Indoleamine 2, 3-dioxygenase
  • Indoleamine-Pyrrole 2,3,-Dioxygenase - biosynthesis
  • Indoleamine-Pyrrole 2,3,-Dioxygenase - drug effects
  • inhaled corticosteroid
  • Kinases
  • kynurenine
  • Macrophages - drug effects
  • Macrophages - enzymology
  • Male
  • Medical sciences
  • Middle Aged
  • Pneumology
  • Proteins
  • Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
  • simvastatin
  • Simvastatin - administration & dosage
  • Simvastatin - therapeutic use
  • Statins
  • Studies
  • Treatment Outcome
  • Universities and colleges
ispartof: Journal of allergy and clinical immunology, 2010, Vol.126 (4), p.754-762.e1
description: Background We have previously shown that inhaled corticosteroids activate indoleamine 2, 3-dioxygenase (IDO) activity through increased IL-10 secretion. Statins might enhance the anti-inflammatory effects of corticosteroids. Objective In a double-blind study we added simvastatin to patients with mild asthma receiving a low dose of inhaled budesonide and evaluated sputum eosinophil counts, IL-10 secretion, and IDO activity, as well as their putative signaling pathways. Methods After a 2-week run-in period without treatment, 50 asthmatic patients were treated with 200 μg of budesonide and randomly assigned to either 10 mg of simvastatin or matched placebo for 8 weeks. Inflammation was evaluated through eosinophil counts, secretory signaling molecules, and immunocytochemistry of macrophages in sputum. Results Sputum eosinophil percentages were reduced significantly by the combined therapy with budesonide and simvastatin compared with budesonide alone ( P  = .02). Corticosteroids activated glucocorticoid-induced TNF receptor ligand, which induces activation of p52 through the noncanonical nuclear factor κB pathway, leading to the increased transcription and activation of IDO. Simvastatin enhanced corticosteroid-activated noncanonical nuclear factor κB–dependent induction of IDO by activating type I interferons and also enhanced the effect of corticosteroid on IL-10 release. Conclusion A statin enhances the anti-inflammatory effect of an inhaled corticosteroid in asthma, and this was mediated through the alteration of IDO activity in macrophages.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0091-6749
fulltext: fulltext
issn:
  • 0091-6749
  • 1097-6825
url: Link


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titleStatins enhance the anti-inflammatory effects of inhaled corticosteroids in asthmatic patients through increased induction of indoleamine 2, 3-dioxygenase
sourceAlma/SFX Local Collection
creatorManeechotesuwan, Kittipong, MD, PhD ; Ekjiratrakul, Wuttichai, MD ; Kasetsinsombat, Kanda, MSc ; Wongkajornsilp, Adisak, MD, PhD ; Barnes, Peter J., DSc, FRS
creatorcontribManeechotesuwan, Kittipong, MD, PhD ; Ekjiratrakul, Wuttichai, MD ; Kasetsinsombat, Kanda, MSc ; Wongkajornsilp, Adisak, MD, PhD ; Barnes, Peter J., DSc, FRS
descriptionBackground We have previously shown that inhaled corticosteroids activate indoleamine 2, 3-dioxygenase (IDO) activity through increased IL-10 secretion. Statins might enhance the anti-inflammatory effects of corticosteroids. Objective In a double-blind study we added simvastatin to patients with mild asthma receiving a low dose of inhaled budesonide and evaluated sputum eosinophil counts, IL-10 secretion, and IDO activity, as well as their putative signaling pathways. Methods After a 2-week run-in period without treatment, 50 asthmatic patients were treated with 200 μg of budesonide and randomly assigned to either 10 mg of simvastatin or matched placebo for 8 weeks. Inflammation was evaluated through eosinophil counts, secretory signaling molecules, and immunocytochemistry of macrophages in sputum. Results Sputum eosinophil percentages were reduced significantly by the combined therapy with budesonide and simvastatin compared with budesonide alone ( P  = .02). Corticosteroids activated glucocorticoid-induced TNF receptor ligand, which induces activation of p52 through the noncanonical nuclear factor κB pathway, leading to the increased transcription and activation of IDO. Simvastatin enhanced corticosteroid-activated noncanonical nuclear factor κB–dependent induction of IDO by activating type I interferons and also enhanced the effect of corticosteroid on IL-10 release. Conclusion A statin enhances the anti-inflammatory effect of an inhaled corticosteroid in asthma, and this was mediated through the alteration of IDO activity in macrophages.
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1EISSN: 1097-6825
2DOI: 10.1016/j.jaci.2010.08.005
3PMID: 20920765
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languageeng
publisherNew York, NY: Mosby, Inc
subjectAbridged Index Medicus ; Adult ; Allergy and Immunology ; Anti-Inflammatory Agents - administration & dosage ; Anti-Inflammatory Agents - therapeutic use ; Anti-inflammatory drugs ; Antiasthmatic agents ; Antitubercular agents ; Asthma ; Asthma - drug therapy ; Biological and medical sciences ; Budesonide - administration & dosage ; Budesonide - therapeutic use ; Cellular biology ; Cholesterol ; Chronic obstructive pulmonary disease, asthma ; Corticosteroids ; Cytokines ; Double-Blind Method ; Drug Synergism ; Drug Therapy, Combination ; Enzyme Induction ; Enzymes ; Female ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Humans ; Immunopathology ; Indoleamine 2, 3-dioxygenase ; Indoleamine-Pyrrole 2,3,-Dioxygenase - biosynthesis ; Indoleamine-Pyrrole 2,3,-Dioxygenase - drug effects ; inhaled corticosteroid ; Kinases ; kynurenine ; Macrophages - drug effects ; Macrophages - enzymology ; Male ; Medical sciences ; Middle Aged ; Pneumology ; Proteins ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; simvastatin ; Simvastatin - administration & dosage ; Simvastatin - therapeutic use ; Statins ; Studies ; Treatment Outcome ; Universities and colleges
ispartofJournal of allergy and clinical immunology, 2010, Vol.126 (4), p.754-762.e1
rights
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3Copyright © 2010 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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1Ekjiratrakul, Wuttichai, MD
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3Wongkajornsilp, Adisak, MD, PhD
4Barnes, Peter J., DSc, FRS
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0Statins enhance the anti-inflammatory effects of inhaled corticosteroids in asthmatic patients through increased induction of indoleamine 2, 3-dioxygenase
1Journal of allergy and clinical immunology
addtitleJ Allergy Clin Immunol
descriptionBackground We have previously shown that inhaled corticosteroids activate indoleamine 2, 3-dioxygenase (IDO) activity through increased IL-10 secretion. Statins might enhance the anti-inflammatory effects of corticosteroids. Objective In a double-blind study we added simvastatin to patients with mild asthma receiving a low dose of inhaled budesonide and evaluated sputum eosinophil counts, IL-10 secretion, and IDO activity, as well as their putative signaling pathways. Methods After a 2-week run-in period without treatment, 50 asthmatic patients were treated with 200 μg of budesonide and randomly assigned to either 10 mg of simvastatin or matched placebo for 8 weeks. Inflammation was evaluated through eosinophil counts, secretory signaling molecules, and immunocytochemistry of macrophages in sputum. Results Sputum eosinophil percentages were reduced significantly by the combined therapy with budesonide and simvastatin compared with budesonide alone ( P  = .02). Corticosteroids activated glucocorticoid-induced TNF receptor ligand, which induces activation of p52 through the noncanonical nuclear factor κB pathway, leading to the increased transcription and activation of IDO. Simvastatin enhanced corticosteroid-activated noncanonical nuclear factor κB–dependent induction of IDO by activating type I interferons and also enhanced the effect of corticosteroid on IL-10 release. Conclusion A statin enhances the anti-inflammatory effect of an inhaled corticosteroid in asthma, and this was mediated through the alteration of IDO activity in macrophages.
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1Adult
2Allergy and Immunology
3Anti-Inflammatory Agents - administration & dosage
4Anti-Inflammatory Agents - therapeutic use
5Anti-inflammatory drugs
6Antiasthmatic agents
7Antitubercular agents
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9Asthma - drug therapy
10Biological and medical sciences
11Budesonide - administration & dosage
12Budesonide - therapeutic use
13Cellular biology
14Cholesterol
15Chronic obstructive pulmonary disease, asthma
16Corticosteroids
17Cytokines
18Double-Blind Method
19Drug Synergism
20Drug Therapy, Combination
21Enzyme Induction
22Enzymes
23Female
24Fundamental and applied biological sciences. Psychology
25Fundamental immunology
26Humans
27Immunopathology
28Indoleamine 2, 3-dioxygenase
29Indoleamine-Pyrrole 2,3,-Dioxygenase - biosynthesis
30Indoleamine-Pyrrole 2,3,-Dioxygenase - drug effects
31inhaled corticosteroid
32Kinases
33kynurenine
34Macrophages - drug effects
35Macrophages - enzymology
36Male
37Medical sciences
38Middle Aged
39Pneumology
40Proteins
41Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
42simvastatin
43Simvastatin - administration & dosage
44Simvastatin - therapeutic use
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48Universities and colleges
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titleStatins enhance the anti-inflammatory effects of inhaled corticosteroids in asthmatic patients through increased induction of indoleamine 2, 3-dioxygenase
authorManeechotesuwan, Kittipong, MD, PhD ; Ekjiratrakul, Wuttichai, MD ; Kasetsinsombat, Kanda, MSc ; Wongkajornsilp, Adisak, MD, PhD ; Barnes, Peter J., DSc, FRS
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1Adult
2Allergy and Immunology
3Anti-Inflammatory Agents - administration & dosage
4Anti-Inflammatory Agents - therapeutic use
5Anti-inflammatory drugs
6Antiasthmatic agents
7Antitubercular agents
8Asthma
9Asthma - drug therapy
10Biological and medical sciences
11Budesonide - administration & dosage
12Budesonide - therapeutic use
13Cellular biology
14Cholesterol
15Chronic obstructive pulmonary disease, asthma
16Corticosteroids
17Cytokines
18Double-Blind Method
19Drug Synergism
20Drug Therapy, Combination
21Enzyme Induction
22Enzymes
23Female
24Fundamental and applied biological sciences. Psychology
25Fundamental immunology
26Humans
27Immunopathology
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29Indoleamine-Pyrrole 2,3,-Dioxygenase - biosynthesis
30Indoleamine-Pyrrole 2,3,-Dioxygenase - drug effects
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40Proteins
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44Simvastatin - therapeutic use
45Statins
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47Treatment Outcome
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atitleStatins enhance the anti-inflammatory effects of inhaled corticosteroids in asthmatic patients through increased induction of indoleamine 2, 3-dioxygenase
jtitleJournal of allergy and clinical immunology
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date2010
risdate2010
volume126
issue4
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epage762.e1
pages754-762.e1
issn0091-6749
eissn1097-6825
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abstractBackground We have previously shown that inhaled corticosteroids activate indoleamine 2, 3-dioxygenase (IDO) activity through increased IL-10 secretion. Statins might enhance the anti-inflammatory effects of corticosteroids. Objective In a double-blind study we added simvastatin to patients with mild asthma receiving a low dose of inhaled budesonide and evaluated sputum eosinophil counts, IL-10 secretion, and IDO activity, as well as their putative signaling pathways. Methods After a 2-week run-in period without treatment, 50 asthmatic patients were treated with 200 μg of budesonide and randomly assigned to either 10 mg of simvastatin or matched placebo for 8 weeks. Inflammation was evaluated through eosinophil counts, secretory signaling molecules, and immunocytochemistry of macrophages in sputum. Results Sputum eosinophil percentages were reduced significantly by the combined therapy with budesonide and simvastatin compared with budesonide alone ( P  = .02). Corticosteroids activated glucocorticoid-induced TNF receptor ligand, which induces activation of p52 through the noncanonical nuclear factor κB pathway, leading to the increased transcription and activation of IDO. Simvastatin enhanced corticosteroid-activated noncanonical nuclear factor κB–dependent induction of IDO by activating type I interferons and also enhanced the effect of corticosteroid on IL-10 release. Conclusion A statin enhances the anti-inflammatory effect of an inhaled corticosteroid in asthma, and this was mediated through the alteration of IDO activity in macrophages.
copNew York, NY
pubMosby, Inc
pmid20920765
doi10.1016/j.jaci.2010.08.005