Targeting Nrf2 signaling improves bacterial clearance by alveolar macrophages in patients with COPD and in a mouse model.
Identifieur interne : 000600 ( PubMed/Checkpoint ); précédent : 000599; suivant : 000601Targeting Nrf2 signaling improves bacterial clearance by alveolar macrophages in patients with COPD and in a mouse model.
Auteurs : Christopher J. Harvey [États-Unis] ; Rajesh K. Thimmulappa ; Sanjay Sethi ; Xiaoni Kong ; Lonny Yarmus ; Robert H. Brown ; David Feller-Kopman ; Robert Wise ; Shyam BiswalSource :
- Science translational medicine [ 1946-6242 ] ; 2011.
Descripteurs français
- KwdFr :
- Adulte d'âge moyen, Animaux, Broncho-pneumopathie chronique obstructive (génétique), Broncho-pneumopathie chronique obstructive (microbiologie), Broncho-pneumopathie chronique obstructive (métabolisme), Cellules cultivées, Facteur-2 apparenté à NF-E2 (génétique), Facteur-2 apparenté à NF-E2 (métabolisme), Femelle, Haemophilus influenzae (pathogénicité), Humains, Isothiocyanates, Macrophages alvéolaires (), Macrophages alvéolaires (microbiologie), Macrophages alvéolaires (métabolisme), Mâle, Phagocytose (), Pseudomonas aeruginosa (pathogénicité), Récepteurs immunologiques (métabolisme), Souris, Sujet âgé, Thiocyanates (usage thérapeutique).
- MESH :
- génétique : Broncho-pneumopathie chronique obstructive, Facteur-2 apparenté à NF-E2.
- microbiologie : Broncho-pneumopathie chronique obstructive, Macrophages alvéolaires.
- métabolisme : Broncho-pneumopathie chronique obstructive, Facteur-2 apparenté à NF-E2, Macrophages alvéolaires, Récepteurs immunologiques.
- pathogénicité : Haemophilus influenzae, Pseudomonas aeruginosa.
- usage thérapeutique : Thiocyanates.
- Adulte d'âge moyen, Animaux, Cellules cultivées, Femelle, Humains, Isothiocyanates, Macrophages alvéolaires, Mâle, Phagocytose, Souris, Sujet âgé.
English descriptors
- KwdEn :
- Aged, Animals, Cells, Cultured, Female, Haemophilus influenzae (pathogenicity), Humans, Isothiocyanates, Macrophages, Alveolar (drug effects), Macrophages, Alveolar (metabolism), Macrophages, Alveolar (microbiology), Male, Mice, Middle Aged, NF-E2-Related Factor 2 (genetics), NF-E2-Related Factor 2 (metabolism), Phagocytosis (drug effects), Pseudomonas aeruginosa (pathogenicity), Pulmonary Disease, Chronic Obstructive (genetics), Pulmonary Disease, Chronic Obstructive (metabolism), Pulmonary Disease, Chronic Obstructive (microbiology), Receptors, Immunologic (metabolism), Thiocyanates (therapeutic use).
- MESH :
- chemical , genetics : NF-E2-Related Factor 2.
- chemical , metabolism : NF-E2-Related Factor 2, Receptors, Immunologic.
- chemical , therapeutic use : Thiocyanates.
- chemical : Isothiocyanates.
- drug effects : Macrophages, Alveolar, Phagocytosis.
- genetics : Pulmonary Disease, Chronic Obstructive.
- metabolism : Macrophages, Alveolar, Pulmonary Disease, Chronic Obstructive.
- microbiology : Macrophages, Alveolar, Pulmonary Disease, Chronic Obstructive.
- pathogenicity : Haemophilus influenzae, Pseudomonas aeruginosa.
- Aged, Animals, Cells, Cultured, Female, Humans, Male, Mice, Middle Aged.
Abstract
Patients with chronic obstructive pulmonary disease (COPD) have innate immune dysfunction in the lung largely due to defective macrophage phagocytosis. This deficiency results in periodic bacterial infections that cause acute exacerbations of COPD, a major source of morbidity and mortality. Recent studies indicate that a decrease in Nrf2 (nuclear erythroid-related factor 2) signaling in patients with COPD may hamper their ability to defend against oxidative stress, although the role of Nrf2 in COPD exacerbations has not been determined. Here, we test whether activation of Nrf2 by the phytochemical sulforaphane restores phagocytosis of clinical isolates of nontypeable Haemophilus influenza (NTHI) and Pseudomonas aeruginosa (PA) by alveolar macrophages from patients with COPD. Sulforaphane treatment restored bacteria recognition and phagocytosis in alveolar macrophages from COPD patients. Furthermore, sulforaphane treatment enhanced pulmonary bacterial clearance by alveolar macrophages and reduced inflammation in wild-type mice but not in Nrf2-deficient mice exposed to cigarette smoke for 6 months. Gene expression and promoter analysis revealed that Nrf2 increased phagocytic ability of macrophages by direct transcriptional up-regulation of the scavenger receptor MARCO. Disruption of Nrf2 or MARCO abrogated sulforaphane-mediated bacterial phagocytosis by COPD alveolar macrophages. Our findings demonstrate the importance of Nrf2 and its downstream target MARCO in improving antibacterial defenses and provide a rationale for targeting this pathway, via pharmacological agents such as sulforaphane, to prevent exacerbations of COPD caused by bacterial infection.
DOI: 10.1126/scitranslmed.3002042
PubMed: 21490276
Affiliations:
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(metabolism)</term><term>Macrophages, Alveolar (microbiology)</term><term>Male</term><term>Mice</term><term>Middle Aged</term><term>NF-E2-Related Factor 2 (genetics)</term><term>NF-E2-Related Factor 2 (metabolism)</term><term>Phagocytosis (drug effects)</term><term>Pseudomonas aeruginosa (pathogenicity)</term><term>Pulmonary Disease, Chronic Obstructive (genetics)</term><term>Pulmonary Disease, Chronic Obstructive (metabolism)</term><term>Pulmonary Disease, Chronic Obstructive (microbiology)</term><term>Receptors, Immunologic (metabolism)</term><term>Thiocyanates (therapeutic use)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte d'âge moyen</term><term>Animaux</term><term>Broncho-pneumopathie chronique obstructive (génétique)</term><term>Broncho-pneumopathie chronique obstructive (microbiologie)</term><term>Broncho-pneumopathie chronique obstructive (métabolisme)</term><term>Cellules cultivées</term><term>Facteur-2 apparenté à NF-E2 (génétique)</term><term>Facteur-2 apparenté à NF-E2 (métabolisme)</term><term>Femelle</term><term>Haemophilus influenzae (pathogénicité)</term><term>Humains</term><term>Isothiocyanates</term><term>Macrophages alvéolaires ()</term><term>Macrophages alvéolaires (microbiologie)</term><term>Macrophages alvéolaires (métabolisme)</term><term>Mâle</term><term>Phagocytose ()</term><term>Pseudomonas aeruginosa (pathogénicité)</term><term>Récepteurs immunologiques (métabolisme)</term><term>Souris</term><term>Sujet âgé</term><term>Thiocyanates (usage thérapeutique)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>NF-E2-Related Factor 2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>NF-E2-Related Factor 2</term><term>Receptors, Immunologic</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Thiocyanates</term></keywords><keywords scheme="MESH" type="chemical" 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qualifier="métabolisme" xml:lang="fr"><term>Broncho-pneumopathie chronique obstructive</term><term>Facteur-2 apparenté à NF-E2</term><term>Macrophages alvéolaires</term><term>Récepteurs immunologiques</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Haemophilus influenzae</term><term>Pseudomonas aeruginosa</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Haemophilus influenzae</term><term>Pseudomonas aeruginosa</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Thiocyanates</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Animals</term><term>Cells, Cultured</term><term>Female</term><term>Humans</term><term>Male</term><term>Mice</term><term>Middle Aged</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte d'âge moyen</term><term>Animaux</term><term>Cellules cultivées</term><term>Femelle</term><term>Humains</term><term>Isothiocyanates</term><term>Macrophages alvéolaires</term><term>Mâle</term><term>Phagocytose</term><term>Souris</term><term>Sujet âgé</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Patients with chronic obstructive pulmonary disease (COPD) have innate immune dysfunction in the lung largely due to defective macrophage phagocytosis. This deficiency results in periodic bacterial infections that cause acute exacerbations of COPD, a major source of morbidity and mortality. Recent studies indicate that a decrease in Nrf2 (nuclear erythroid-related factor 2) signaling in patients with COPD may hamper their ability to defend against oxidative stress, although the role of Nrf2 in COPD exacerbations has not been determined. Here, we test whether activation of Nrf2 by the phytochemical sulforaphane restores phagocytosis of clinical isolates of nontypeable Haemophilus influenza (NTHI) and Pseudomonas aeruginosa (PA) by alveolar macrophages from patients with COPD. Sulforaphane treatment restored bacteria recognition and phagocytosis in alveolar macrophages from COPD patients. Furthermore, sulforaphane treatment enhanced pulmonary bacterial clearance by alveolar macrophages and reduced inflammation in wild-type mice but not in Nrf2-deficient mice exposed to cigarette smoke for 6 months. Gene expression and promoter analysis revealed that Nrf2 increased phagocytic ability of macrophages by direct transcriptional up-regulation of the scavenger receptor MARCO. Disruption of Nrf2 or MARCO abrogated sulforaphane-mediated bacterial phagocytosis by COPD alveolar macrophages. Our findings demonstrate the importance of Nrf2 and its downstream target MARCO in improving antibacterial defenses and provide a rationale for targeting this pathway, via pharmacological agents such as sulforaphane, to prevent exacerbations of COPD caused by bacterial infection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21490276</PMID><DateCompleted><Year>2011</Year><Month>08</Month><Day>03</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1946-6242</ISSN><JournalIssue CitedMedium="Internet"><Volume>3</Volume><Issue>78</Issue><PubDate><Year>2011</Year><Month>Apr</Month><Day>13</Day></PubDate></JournalIssue><Title>Science translational medicine</Title><ISOAbbreviation>Sci Transl Med</ISOAbbreviation></Journal><ArticleTitle>Targeting Nrf2 signaling improves bacterial clearance by alveolar macrophages in patients with COPD and in a mouse model.</ArticleTitle><Pagination><MedlinePgn>78ra32</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1126/scitranslmed.3002042</ELocationID><Abstract><AbstractText>Patients with chronic obstructive pulmonary disease (COPD) have innate immune dysfunction in the lung largely due to defective macrophage phagocytosis. This deficiency results in periodic bacterial infections that cause acute exacerbations of COPD, a major source of morbidity and mortality. Recent studies indicate that a decrease in Nrf2 (nuclear erythroid-related factor 2) signaling in patients with COPD may hamper their ability to defend against oxidative stress, although the role of Nrf2 in COPD exacerbations has not been determined. Here, we test whether activation of Nrf2 by the phytochemical sulforaphane restores phagocytosis of clinical isolates of nontypeable Haemophilus influenza (NTHI) and Pseudomonas aeruginosa (PA) by alveolar macrophages from patients with COPD. Sulforaphane treatment restored bacteria recognition and phagocytosis in alveolar macrophages from COPD patients. Furthermore, sulforaphane treatment enhanced pulmonary bacterial clearance by alveolar macrophages and reduced inflammation in wild-type mice but not in Nrf2-deficient mice exposed to cigarette smoke for 6 months. Gene expression and promoter analysis revealed that Nrf2 increased phagocytic ability of macrophages by direct transcriptional up-regulation of the scavenger receptor MARCO. Disruption of Nrf2 or MARCO abrogated sulforaphane-mediated bacterial phagocytosis by COPD alveolar macrophages. Our findings demonstrate the importance of Nrf2 and its downstream target MARCO in improving antibacterial defenses and provide a rationale for targeting this pathway, via pharmacological agents such as sulforaphane, to prevent exacerbations of COPD caused by bacterial infection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Harvey</LastName><ForeName>Christopher J</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, MD 21205, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thimmulappa</LastName><ForeName>Rajesh K</ForeName><Initials>RK</Initials></Author><Author ValidYN="Y"><LastName>Sethi</LastName><ForeName>Sanjay</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Kong</LastName><ForeName>Xiaoni</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>Yarmus</LastName><ForeName>Lonny</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Brown</LastName><ForeName>Robert H</ForeName><Initials>RH</Initials></Author><Author ValidYN="Y"><LastName>Feller-Kopman</LastName><ForeName>David</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Wise</LastName><ForeName>Robert</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Biswal</LastName><ForeName>Shyam</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P50ES015903</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 ES015903</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P01 HL010342</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL10342</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>ES07141</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL081205</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 HL084945</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50HL084945</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>ES03819</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL081205</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 ES007141</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 ES003819</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Sci Transl Med</MedlineTA><NlmUniqueID>101505086</NlmUniqueID><ISSNLinking>1946-6234</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017879">Isothiocyanates</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011971">Receptors, Immunologic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013861">Thiocyanates</NameOfSubstance></Chemical><Chemical><RegistryNumber>GA49J4310U</RegistryNumber><NameOfSubstance UI="C016766">sulforafan</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006193" MajorTopicYN="N">Haemophilus influenzae</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017879" MajorTopicYN="N">Isothiocyanates</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016676" MajorTopicYN="N">Macrophages, Alveolar</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051267" MajorTopicYN="N">NF-E2-Related Factor 2</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010587" MajorTopicYN="N">Phagocytosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011550" MajorTopicYN="N">Pseudomonas aeruginosa</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029424" MajorTopicYN="N">Pulmonary Disease, Chronic Obstructive</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011971" MajorTopicYN="N">Receptors, Immunologic</DescriptorName><QualifierName UI="Q000378" 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