Cellular and Molecular Connections between Autophagy and Inflammation
Identifieur interne : 000113 ( Pmc/Curation ); précédent : 000112; suivant : 000114Cellular and Molecular Connections between Autophagy and Inflammation
Auteurs : Pierre Lapaquette [France] ; Jean Guzzo [France] ; Lionel Bretillon [France] ; Marie-Agnès Bringer [France]Source :
- Mediators of Inflammation [ 0962-9351 ] ; 2015.
Abstract
Autophagy is an intracellular catabolic pathway essential for the recycling of proteins and larger substrates such as aggregates, apoptotic corpses, or long-lived and superfluous organelles whose accumulation could be toxic for cells. Because of its unique feature to engulf part of cytoplasm in double-membrane cup-shaped structures, which further fuses with lysosomes, autophagy is also involved in the elimination of host cell invaders and takes an active part of the innate and adaptive immune response. Its pivotal role in maintenance of the inflammatory balance makes dysfunctions of the autophagy process having important pathological consequences. Indeed, defects in autophagy are associated with a wide range of human diseases including metabolic disorders (diabetes and obesity), inflammatory bowel disease (IBD), and cancer. In this review, we will focus on interrelations that exist between inflammation and autophagy. We will discuss in particular how mediators of inflammation can regulate autophagy activity and, conversely, how autophagy shapes the inflammatory response. Impact of genetic polymorphisms in autophagy-related gene on inflammatory bowel disease will be also discussed.
Url:
DOI: 10.1155/2015/398483
PubMed: 26221063
PubMed Central: 4499609
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<front><div type="abstract" xml:lang="en"><p>Autophagy is an intracellular catabolic pathway essential for the recycling of proteins and larger substrates such as aggregates, apoptotic corpses, or long-lived and superfluous organelles whose accumulation could be toxic for cells. Because of its unique feature to engulf part of cytoplasm in double-membrane cup-shaped structures, which further fuses with lysosomes, autophagy is also involved in the elimination of host cell invaders and takes an active part of the innate and adaptive immune response. Its pivotal role in maintenance of the inflammatory balance makes dysfunctions of the autophagy process having important pathological consequences. Indeed, defects in autophagy are associated with a wide range of human diseases including metabolic disorders (diabetes and obesity), inflammatory bowel disease (IBD), and cancer. In this review, we will focus on interrelations that exist between inflammation and autophagy. We will discuss in particular how mediators of inflammation can regulate autophagy activity and, conversely, how autophagy shapes the inflammatory response. Impact of genetic polymorphisms in autophagy-related gene on inflammatory bowel disease will be also discussed.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Mediators Inflamm</journal-id>
<journal-id journal-id-type="iso-abbrev">Mediators Inflamm</journal-id>
<journal-id journal-id-type="publisher-id">MI</journal-id>
<journal-title-group><journal-title>Mediators of Inflammation</journal-title>
</journal-title-group>
<issn pub-type="ppub">0962-9351</issn>
<issn pub-type="epub">1466-1861</issn>
<publisher><publisher-name>Hindawi Publishing Corporation</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">26221063</article-id>
<article-id pub-id-type="pmc">4499609</article-id>
<article-id pub-id-type="doi">10.1155/2015/398483</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Cellular and Molecular Connections between Autophagy and Inflammation</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Lapaquette</surname>
<given-names>Pierre</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="I2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Guzzo</surname>
<given-names>Jean</given-names>
</name>
<xref ref-type="aff" rid="I1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="I2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bretillon</surname>
<given-names>Lionel</given-names>
</name>
<xref ref-type="aff" rid="I3"><sup>3</sup>
</xref>
<xref ref-type="aff" rid="I4"><sup>4</sup>
</xref>
<xref ref-type="aff" rid="I5"><sup>5</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bringer</surname>
<given-names>Marie-Agnès</given-names>
</name>
<xref ref-type="aff" rid="I3"><sup>3</sup>
</xref>
<xref ref-type="aff" rid="I4"><sup>4</sup>
</xref>
<xref ref-type="aff" rid="I5"><sup>5</sup>
</xref>
<xref ref-type="corresp" rid="cor1"><sup>*</sup>
</xref>
</contrib>
</contrib-group>
<aff id="I1"><sup>1</sup>
Université Bourgogne Franche-Comté, UMR PAM, Équipe Vin, Aliment, Microbiologie, Stress, 21000 Dijon, France</aff>
<aff id="I2"><sup>2</sup>
Agrosup Dijon, UMR PAM, Équipe Vin, Aliment, Microbiologie, Stress, 21000 Dijon, France</aff>
<aff id="I3"><sup>3</sup>
INRA, UMR1324 Centre des Sciences du Goût et de l'Alimentation, 21000 Dijon, France</aff>
<aff id="I4"><sup>4</sup>
CNRS, UMR6265 Centre des Sciences du Goût et de l'Alimentation, 21000 Dijon, France</aff>
<aff id="I5"><sup>5</sup>
Université Bourgogne Franche-Comté, Centre des Sciences du Goût et de l'Alimentation, 21000 Dijon, France</aff>
<author-notes><corresp id="cor1">*Marie-Agnès Bringer: <email>marie-agnes.bringer@dijon.inra.fr</email>
</corresp>
<fn fn-type="other"><p>Academic Editor: Dmitri V. Krysko</p>
</fn>
</author-notes>
<pub-date pub-type="ppub"><year>2015</year>
</pub-date>
<pub-date pub-type="epub"><day>29</day>
<month>6</month>
<year>2015</year>
</pub-date>
<volume>2015</volume>
<elocation-id>398483</elocation-id>
<history><date date-type="received"><day>15</day>
<month>3</month>
<year>2015</year>
</date>
<date date-type="rev-recd"><day>2</day>
<month>6</month>
<year>2015</year>
</date>
<date date-type="accepted"><day>14</day>
<month>6</month>
<year>2015</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2015 Pierre Lapaquette et al.</copyright-statement>
<copyright-year>2015</copyright-year>
<license license-type="open-access"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
</license>
</permissions>
<abstract><p>Autophagy is an intracellular catabolic pathway essential for the recycling of proteins and larger substrates such as aggregates, apoptotic corpses, or long-lived and superfluous organelles whose accumulation could be toxic for cells. Because of its unique feature to engulf part of cytoplasm in double-membrane cup-shaped structures, which further fuses with lysosomes, autophagy is also involved in the elimination of host cell invaders and takes an active part of the innate and adaptive immune response. Its pivotal role in maintenance of the inflammatory balance makes dysfunctions of the autophagy process having important pathological consequences. Indeed, defects in autophagy are associated with a wide range of human diseases including metabolic disorders (diabetes and obesity), inflammatory bowel disease (IBD), and cancer. In this review, we will focus on interrelations that exist between inflammation and autophagy. We will discuss in particular how mediators of inflammation can regulate autophagy activity and, conversely, how autophagy shapes the inflammatory response. Impact of genetic polymorphisms in autophagy-related gene on inflammatory bowel disease will be also discussed.</p>
</abstract>
</article-meta>
</front>
<floats-group><fig id="fig1" orientation="portrait" position="float"><label>Figure 1</label>
<caption><p>Autophagy and inflammation. By integrating output signals from PRRs (brown box), cytokines, and chemokines (blue box) and ROS (orange box), autophagy regulatory network is able to dynamically respond to inflammation. Transcriptionally, inflammation-related transcription factors shape transcriptional program of autophagy (grey box). Active autophagy reduces inflammation at least by mediating damaged organelles clearance, lowering microorganisms intracellular load and degrading inflammatory mediators (red box).</p>
</caption>
<graphic xlink:href="MI2015-398483.001"></graphic>
</fig>
</floats-group>
</pmc>
</record>
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