Aspects of Autophagy in Inflammatory Bowel Disease

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Autophagy Networks in Inflammation

Part of the book series: Progress in Inflammation Research ((PIR))

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Abstract

Crohn’s disease and ulcerative colitis the main clinical phenotypes of inflammatory bowel disease are polygenic immune disorders with multifactorial etiology. Recent genome-wide association studies have highlighted on the importance of the autophagy pathway. Thus, autophagy is now widely considered as a key regulator mechanism with the capacity to integrate several aspects of Crohn’s disease pathogenesis. Chronic, unchecked inflammation has widely been suggested to trigger carcinogenesis. In addition, accumulating evidence indicates that the aberrantly altered process of autophagy is definitely involved in carcinogenesis, as well. Toll-like receptors sensing cell-derived pattern/danger-associated molecules also have the capacity to promote tumor development and immune escape. However, both TLR- and autophagy-related signals may exert tumor suppressor mechanisms mainly in a cell-specific and context-dependent manner. Though the precise impact of autophagy in inflammatory bowel disease and on inflammation (colitis)-associated cancer has not yet been clarified, it may indicate a novel promising therapeutic aspect.

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Abbreviations

AIEC:

Adherent-invasive Escherichia coli

AKT:

Protein kinase B (PKB)

AOM:

Azoxymethane

APCs:

Antigen-presenting cells

APP:

Amyloid-β precursor protein

Atg:

Autophagy-related

ATP:

Adenosine triphosphate

Bcl-2:

B-cell lymphoma 2

Bcl-xL:

B-cell lymphoma-extra large

Bif-1:

Bax-binding protein-1

CAC:

Colitis-associated cancer

CALCOCO2/NDP52:

Autophagy receptor calcium binding and coiled-coil domain 2

CAMP:

Cyclic adenosine monophosphate

CARD:

Caspase activation and recruitment domain

CD:

Crohn’s disease

COX:

Cyclooxygenase

DAMP:

Damage-associated molecular pattern

DCs:

Dendritic cells

DSS:

Dextran sulfate sodium

EGFR:

Epidermal growth factor receptor

ER:

Endoplasmatic reticulum

FAK:

Focal Adhesion Kinase

FIP200:

FAK family kinase-interacting protein of 200 kDa

GI:

Gastrointestinal

GO:

Graphene oxide

GTP:

Guanosine-5′-triphosphate

HMGB-1:

High-mobility-group B-1

HSP:

Heat-schock protein

IBD:

Inflammatory bowel disease

ICD:

Immunogenic cell death

IECs:

Intestinal epithelial cells

IFN:

Interferon

IKK:

Inhibitor of κB-kinase

IL:

Interleukine

IP3:

Inositol triphosphate

IRAKs:

Interleukin-1 receptor-associated kinases

IRE1/XBP1:

Inositol-requiring enzyme 1/X-box binding protein 1

IRF:

Interferon regulatory factor

IRGM:

Immunity-related GTPase family M protein

JNKs:

c-Jun N-terminal kinases

LC3:

Microtubule-associated protein 1A/1B-light chain 3

LP:

Lamina propria

LPS:

Lipopolysaccharide

LRR:

Leucine-rich repeat

MAPK:

Mitogen-activated protein kinases

MDP:

N-acetyl-muramyl-peptide

MHC:

Major histocompatibility complex

mTORC1:

Mammalian TOR complex 1

MyD88:

Myeloid differentiation primary response gene 88

NF-κB:

Nuclear factor-κB

NLRP3:

NOD-like receptor family, pyrin domain containing 3

NLRs:

NOD-like receptors

NOD2:

Nucleotide-binding oligomerization domain containing protein 2

ODN:

Oligodeoxynucleotide

PAMPs:

Pathogen-associated molecular patterns

PARP:

Poly-ADP-ribose polymerase

pDCs:

Plasmocytoid DCs

PG:

Prostaglandin

PI3K:

Phosphatidylinositol-4,5-bisphosphate 3-kinase

PRRs:

Pattern recognition receptors

PTPN22:

Protein tyrosine phosphatase non-receptor type 22

RIG:

Retinoic acid-inducible gene 1

RIP2:

Receptor interacting protein 2

RLRs:

RIG-I-like receptors

ROS:

Reactive oxygen species

SNP:

Single nucleotide polymorphisms

STAT:

Signal transducer and activator of transcription

TCD:

Tolerogenic cell death

TIR:

Toll/interleukin-1 receptor

TLR:

Toll-like receptor

TNF:

Tumor necrosis factor

TOR:

Target of rapamycin

TRAF:

TNF-receptor-associated factor

TRAM:

Toll-like receptor 4 adaptor protein

Treg:

Regulatory T cells

TRIF:

TIR-domain-containing adapter-inducing interferon-β

UC:

Ulcerative colitis

UPR:

Unfolded protein response

UVRAG:

UV radiation resistance-associated gene protein.

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Sipos, F., Műzes, G. (2016). Aspects of Autophagy in Inflammatory Bowel Disease. In: Maiuri, M., De Stefano, D. (eds) Autophagy Networks in Inflammation. Progress in Inflammation Research. Springer, Cham. https://doi.org/10.1007/978-3-319-30079-5_12

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  • DOI: https://doi.org/10.1007/978-3-319-30079-5_12

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