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Cellular and Molecular Connections between Autophagy and Inflammation.

Lapaquette P, Guzzo J, Bretillon L, Bringer MA - Mediators Inflamm. (2015)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Université Bourgogne Franche-Comté, UMR PAM, Équipe Vin, Aliment, Microbiologie, Stress, 21000 Dijon, France ; Agrosup Dijon, UMR PAM, Équipe Vin, Aliment, Microbiologie, Stress, 21000 Dijon, France.

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.

No MeSH data available.


Related in: MedlinePlus

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).
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Related In: Results  -  Collection


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fig1: 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).

Mentions: As illustrated by studies detailed above in this review, autophagy and autophagy-related proteins are essential components modulating inflammatory response either directly by acting on stability or secretion of inflammatory mediators or indirectly by suppressing intracellular stressors (e.g., damaged organelles, intracellular pathogenic microorganisms, and ER stress). Autophagy regulatory network integrates a wide range of signals from innate immune receptors sensing PAMPs (TLRs and NLRs), cytokines, and ROS and thereby is able to respond appropriately according to the degree of inflammatory state (Figure 1).


Cellular and Molecular Connections between Autophagy and Inflammation.

Lapaquette P, Guzzo J, Bretillon L, Bringer MA - Mediators Inflamm. (2015)

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).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4499609&req=5

fig1: 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).
Mentions: As illustrated by studies detailed above in this review, autophagy and autophagy-related proteins are essential components modulating inflammatory response either directly by acting on stability or secretion of inflammatory mediators or indirectly by suppressing intracellular stressors (e.g., damaged organelles, intracellular pathogenic microorganisms, and ER stress). Autophagy regulatory network integrates a wide range of signals from innate immune receptors sensing PAMPs (TLRs and NLRs), cytokines, and ROS and thereby is able to respond appropriately according to the degree of inflammatory state (Figure 1).

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Université Bourgogne Franche-Comté, UMR PAM, Équipe Vin, Aliment, Microbiologie, Stress, 21000 Dijon, France ; Agrosup Dijon, UMR PAM, Équipe Vin, Aliment, Microbiologie, Stress, 21000 Dijon, France.

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.

No MeSH data available.


Related in: MedlinePlus