RapamycinFungusV1, Main, Exploration, bibRecord, 000C85

Hypercapnia Inhibits Autophagy and Bacterial Killing in Human Macrophages by Increasing Expression of Bcl-2 and Bcl-xL.

Identifieur interne : 000C85 ( Main/Exploration ); précédent : 000C84; suivant : 000C86

Hypercapnia Inhibits Autophagy and Bacterial Killing in Human Macrophages by Increasing Expression of Bcl-2 and Bcl-xL.

Auteurs : S Marina Casalino-Matsuda [États-Unis] ; Aisha Nair [États-Unis] ; Greg J. Beitel [États-Unis] ; Khalilah L. Gates [États-Unis] ; Peter H S. Sporn [États-Unis]

Source :

Journal of immunology (Baltimore, Md. : 1950) [ 1550-6606 ] ; 2015.

RBID : pubmed:25895534

Descripteurs français

KwdFr :
- Acidose (MeSH), Animaux (MeSH), Autophagie (effets des médicaments et des substances chimiques), Autophagie (immunologie), Bécline-1 (MeSH), Dioxyde de carbone (pharmacologie), Dioxyde de carbone (sang), Humains (MeSH), Hypercapnie (immunologie), Hypercapnie (sang), Indoles (pharmacologie), Interférence par ARN (MeSH), Liaison aux protéines (effets des médicaments et des substances chimiques), Lignée cellulaire (MeSH), Lipopolysaccharides (MeSH), Macrophages alvéolaires (immunologie), Macrophages alvéolaires (microbiologie), Maladies pulmonaires (anatomopathologie), Petit ARN interférent (MeSH), Phagocytose (effets des médicaments et des substances chimiques), Protéine bcl-X (biosynthèse), Protéine bcl-X (génétique), Protéines membranaires (antagonistes et inhibiteurs), Protéines proto-oncogènes c-bcl-2 (biosynthèse), Protéines proto-oncogènes c-bcl-2 (génétique), Protéines régulatrices de l'apoptose (antagonistes et inhibiteurs), Pseudomonas aeruginosa (immunologie), Sirolimus (pharmacologie), Souris (MeSH).
MESH :
- anatomopathologie : Maladies pulmonaires.
- antagonistes et inhibiteurs : Protéines membranaires, Protéines régulatrices de l'apoptose.
- biosynthèse : Protéine bcl-X, Protéines proto-oncogènes c-bcl-2.
- effets des médicaments et des substances chimiques : Autophagie, Liaison aux protéines, Phagocytose.
- génétique : Protéine bcl-X, Protéines proto-oncogènes c-bcl-2.
- immunologie : Autophagie, Hypercapnie, Macrophages alvéolaires, Pseudomonas aeruginosa.
- microbiologie : Macrophages alvéolaires.
- pharmacologie : Dioxyde de carbone, Indoles, Sirolimus.
- sang : Dioxyde de carbone, Hypercapnie.
- Acidose, Animaux, Bécline-1, Humains, Interférence par ARN, Lignée cellulaire, Lipopolysaccharides, Petit ARN interférent, Souris.

English descriptors

KwdEn :
- Acidosis (MeSH), Animals (MeSH), Apoptosis Regulatory Proteins (antagonists & inhibitors), Autophagy (drug effects), Autophagy (immunology), Beclin-1 (MeSH), Carbon Dioxide (blood), Carbon Dioxide (pharmacology), Cell Line (MeSH), Humans (MeSH), Hypercapnia (blood), Hypercapnia (immunology), Indoles (pharmacology), Lipopolysaccharides (MeSH), Lung Diseases (pathology), Macrophages, Alveolar (immunology), Macrophages, Alveolar (microbiology), Membrane Proteins (antagonists & inhibitors), Mice (MeSH), Phagocytosis (drug effects), Protein Binding (drug effects), Proto-Oncogene Proteins c-bcl-2 (biosynthesis), Proto-Oncogene Proteins c-bcl-2 (genetics), Pseudomonas aeruginosa (immunology), RNA Interference (MeSH), RNA, Small Interfering (MeSH), Sirolimus (pharmacology), bcl-X Protein (biosynthesis), bcl-X Protein (genetics).
MESH :
- chemical , antagonists & inhibitors : Apoptosis Regulatory Proteins, Membrane Proteins.
- chemical , biosynthesis : Proto-Oncogene Proteins c-bcl-2, bcl-X Protein.
- chemical , blood : Carbon Dioxide.
- blood : Hypercapnia.
- drug effects : Autophagy, Phagocytosis, Protein Binding.
- chemical , genetics : Proto-Oncogene Proteins c-bcl-2, bcl-X Protein.
- immunology : Autophagy, Hypercapnia, Macrophages, Alveolar, Pseudomonas aeruginosa.
- microbiology : Macrophages, Alveolar.
- pathology : Lung Diseases.
- chemical , pharmacology : Carbon Dioxide, Indoles, Sirolimus.
- Acidosis, Animals, Beclin-1, Cell Line, Humans, Lipopolysaccharides, Mice, RNA Interference, RNA, Small Interfering.

Abstract

Hypercapnia, the elevation of CO2 in blood and tissue, commonly develops in patients with advanced lung disease and severe pulmonary infections, and it is associated with high mortality. We previously reported that hypercapnia alters expression of host defense genes, inhibits phagocytosis, and increases the mortality of Pseudomonas pneumonia in mice. However, the effect of hypercapnia on autophagy, a conserved process by which cells sequester and degrade proteins and damaged organelles that also plays a key role in antimicrobial host defense and pathogen clearance, has not previously been examined. In the present study we show that hypercapnia inhibits autophagy induced by starvation, rapamycin, LPS, heat-killed bacteria, and live bacteria in the human macrophage. Inhibition of autophagy by elevated CO2 was not attributable to acidosis. Hypercapnia also reduced macrophage killing of Pseudomonas aeruginosa. Moreover, elevated CO2 induced the expression of Bcl-2 and Bcl-xL, antiapoptotic factors that negatively regulate autophagy by blocking Beclin 1, an essential component of the autophagy initiation complex. Furthermore, small interfering RNA targeting Bcl-2 and Bcl-xL and the small molecule Z36, which blocks Bcl-2 and Bcl-xL binding to Beclin 1, prevented hypercapnic inhibition of autophagy and bacterial killing. These results suggest that targeting the Bcl-2/Bcl-xL-Beclin 1 interaction may hold promise for ameliorating hypercapnia-induced immunosuppression and improving resistance to infection in patients with advanced lung disease and hypercapnia.

DOI: 10.4049/jimmunol.1500150
PubMed: 25895534
PubMed Central: PMC4433787

Affiliations:

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Le document en format XML

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<term>Apoptosis Regulatory Proteins (antagonists & inhibitors)</term>
<term>Autophagy (drug effects)</term>
<term>Autophagy (immunology)</term>
<term>Beclin-1 (MeSH)</term>
<term>Carbon Dioxide (blood)</term>
<term>Carbon Dioxide (pharmacology)</term>
<term>Cell Line (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Hypercapnia (blood)</term>
<term>Hypercapnia (immunology)</term>
<term>Indoles (pharmacology)</term>
<term>Lipopolysaccharides (MeSH)</term>
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<term>Macrophages, Alveolar (immunology)</term>
<term>Macrophages, Alveolar (microbiology)</term>
<term>Membrane Proteins (antagonists & inhibitors)</term>
<term>Mice (MeSH)</term>
<term>Phagocytosis (drug effects)</term>
<term>Protein Binding (drug effects)</term>
<term>Proto-Oncogene Proteins c-bcl-2 (biosynthesis)</term>
<term>Proto-Oncogene Proteins c-bcl-2 (genetics)</term>
<term>Pseudomonas aeruginosa (immunology)</term>
<term>RNA Interference (MeSH)</term>
<term>RNA, Small Interfering (MeSH)</term>
<term>Sirolimus (pharmacology)</term>
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<term>bcl-X Protein (genetics)</term>
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<term>Animaux (MeSH)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Autophagie (immunologie)</term>
<term>Bécline-1 (MeSH)</term>
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<term>Dioxyde de carbone (sang)</term>
<term>Humains (MeSH)</term>
<term>Hypercapnie (immunologie)</term>
<term>Hypercapnie (sang)</term>
<term>Indoles (pharmacologie)</term>
<term>Interférence par ARN (MeSH)</term>
<term>Liaison aux protéines (effets des médicaments et des substances chimiques)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lipopolysaccharides (MeSH)</term>
<term>Macrophages alvéolaires (immunologie)</term>
<term>Macrophages alvéolaires (microbiologie)</term>
<term>Maladies pulmonaires (anatomopathologie)</term>
<term>Petit ARN interférent (MeSH)</term>
<term>Phagocytose (effets des médicaments et des substances chimiques)</term>
<term>Protéine bcl-X (biosynthèse)</term>
<term>Protéine bcl-X (génétique)</term>
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<term>Protéines proto-oncogènes c-bcl-2 (génétique)</term>
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<term>Pseudomonas aeruginosa (immunologie)</term>
<term>Sirolimus (pharmacologie)</term>
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<term>Membrane Proteins</term>
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<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Proto-Oncogene Proteins c-bcl-2</term>
<term>bcl-X Protein</term>
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<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Carbon Dioxide</term>
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<term>Protéines proto-oncogènes c-bcl-2</term>
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<term>Phagocytose</term>
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<term>Pseudomonas aeruginosa</term>
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<term>Hypercapnia</term>
<term>Macrophages, Alveolar</term>
<term>Pseudomonas aeruginosa</term>
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</keywords>
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<term>Indoles</term>
<term>Sirolimus</term>
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<term>Sirolimus</term>
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<term>Animals</term>
<term>Beclin-1</term>
<term>Cell Line</term>
<term>Humans</term>
<term>Lipopolysaccharides</term>
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<term>Animaux</term>
<term>Bécline-1</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire</term>
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<front><div type="abstract" xml:lang="en">Hypercapnia, the elevation of CO2 in blood and tissue, commonly develops in patients with advanced lung disease and severe pulmonary infections, and it is associated with high mortality. We previously reported that hypercapnia alters expression of host defense genes, inhibits phagocytosis, and increases the mortality of Pseudomonas pneumonia in mice. However, the effect of hypercapnia on autophagy, a conserved process by which cells sequester and degrade proteins and damaged organelles that also plays a key role in antimicrobial host defense and pathogen clearance, has not previously been examined. In the present study we show that hypercapnia inhibits autophagy induced by starvation, rapamycin, LPS, heat-killed bacteria, and live bacteria in the human macrophage. Inhibition of autophagy by elevated CO2 was not attributable to acidosis. Hypercapnia also reduced macrophage killing of Pseudomonas aeruginosa. Moreover, elevated CO2 induced the expression of Bcl-2 and Bcl-xL, antiapoptotic factors that negatively regulate autophagy by blocking Beclin 1, an essential component of the autophagy initiation complex. Furthermore, small interfering RNA targeting Bcl-2 and Bcl-xL and the small molecule Z36, which blocks Bcl-2 and Bcl-xL binding to Beclin 1, prevented hypercapnic inhibition of autophagy and bacterial killing. These results suggest that targeting the Bcl-2/Bcl-xL-Beclin 1 interaction may hold promise for ameliorating hypercapnia-induced immunosuppression and improving resistance to infection in patients with advanced lung disease and hypercapnia. </div>
</front>
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<Month>11</Month>
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<Title>Journal of immunology (Baltimore, Md. : 1950)</Title>
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<Abstract><AbstractText>Hypercapnia, the elevation of CO2 in blood and tissue, commonly develops in patients with advanced lung disease and severe pulmonary infections, and it is associated with high mortality. We previously reported that hypercapnia alters expression of host defense genes, inhibits phagocytosis, and increases the mortality of Pseudomonas pneumonia in mice. However, the effect of hypercapnia on autophagy, a conserved process by which cells sequester and degrade proteins and damaged organelles that also plays a key role in antimicrobial host defense and pathogen clearance, has not previously been examined. In the present study we show that hypercapnia inhibits autophagy induced by starvation, rapamycin, LPS, heat-killed bacteria, and live bacteria in the human macrophage. Inhibition of autophagy by elevated CO2 was not attributable to acidosis. Hypercapnia also reduced macrophage killing of Pseudomonas aeruginosa. Moreover, elevated CO2 induced the expression of Bcl-2 and Bcl-xL, antiapoptotic factors that negatively regulate autophagy by blocking Beclin 1, an essential component of the autophagy initiation complex. Furthermore, small interfering RNA targeting Bcl-2 and Bcl-xL and the small molecule Z36, which blocks Bcl-2 and Bcl-xL binding to Beclin 1, prevented hypercapnic inhibition of autophagy and bacterial killing. These results suggest that targeting the Bcl-2/Bcl-xL-Beclin 1 interaction may hold promise for ameliorating hypercapnia-induced immunosuppression and improving resistance to infection in patients with advanced lung disease and hypercapnia. </AbstractText>
<CopyrightInformation>Copyright © 2015 by The American Association of Immunologists, Inc.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Casalino-Matsuda</LastName>
<ForeName>S Marina</ForeName>
<Initials>SM</Initials>
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<AffiliationInfo><Affiliation>Department of Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611; marinamatsuda@northwestern.edu.</Affiliation>
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<Author ValidYN="Y"><LastName>Nair</LastName>
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<Acronym>BX</Acronym>
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Serveur d'exploration sur la rapamycine et les champignons

Hypercapnia Inhibits Autophagy and Bacterial Killing in Human Macrophages by Increasing Expression of Bcl-2 and Bcl-xL.

Hypercapnia Inhibits Autophagy and Bacterial Killing in Human Macrophages by Increasing Expression of Bcl-2 and Bcl-xL.

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