TLR4-mediated autophagy in macrophages is a p62-dependent type of selective autophagy of aggresome-like induced structures (ALIS)

Autophagy plays an evolutionarily conserved role in host defense against pathogens. Autophagic protection mechanisms against microbes range from regulating immune signaling responses to directly targeting the pathogens for lysosomal degradation. Toll-like receptors (TLRs) that detect conserved molec...

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Bibliographic Details
Published in:Autophagy 2011-05, Vol.7 (5), p.552-554
Main Authors: Fujita, Ken-Ichi, Srinivasula, Srinivasa M.
Format: Article
Language:English
Subjects:
Adaptor Proteins, Signal Transducing - genetics
Adaptor Proteins, Signal Transducing - metabolism
Adaptor Proteins, Signal Transducing - physiology
Animals
Autophagic Punctum
Autophagy - drug effects
Autophagy - genetics
Autophagy - physiology
Binding
Biology
Bioscience
Calcium
Cancer
Cell
Cycle
Humans
Immunity, Innate - drug effects
Immunity, Innate - genetics
Immunity, Innate - physiology
Inclusion Bodies - drug effects
Inclusion Bodies - metabolism
Inclusion Bodies - physiology
Landes
Lipopolysaccharides - pharmacology
Macrophages - drug effects
Macrophages - metabolism
Macrophages - physiology
Models, Biological
Organogenesis
Proteins
Sequestosome-1 Protein
Toll-Like Receptor 4 - genetics
Toll-Like Receptor 4 - physiology
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Summary:Autophagy plays an evolutionarily conserved role in host defense against pathogens. Autophagic protection mechanisms against microbes range from regulating immune signaling responses to directly targeting the pathogens for lysosomal degradation. Toll-like receptors (TLRs) that detect conserved molecular features shared by pathogens regulate several innate immune responses including autophagy. Our recent study demonstrates that autophagy reported in response to TLR4-stimulation in macrophages is selective autophagy of aggresome-like induced structures (ALIS), and p62 (also known as SQSTM1) plays an essential role in this process. Treatment of macrophages with either Escherichia coli or lipopolysaccharide (LPS) results in the activation of nuclear factor erythroid 2-related factor 2 (Nrf2), leading to an increase in the levels of p62 mRNA and protein, assembly of ALIS and their autophagic degradation. This study revealed a signaling role for p62, distinct from its known function as a bacterial-targeting factor, which might be critical for cellular stress response during infection.
ISSN:1554-8627
1554-8635
DOI:10.4161/auto.7.5.15101