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Cited by 52Inflammasome and immune disordersImmune Response and InflammationPlant-Microbe Interactions and Immunity

The role of the inflammasome in cellular responses to toxins and bacterial effectors

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Freche, Barbara, Reig, Núria, van der Goot, F. Gisou·2007·Seminars in Immunopathology
DOI 10.1007/s00281-007-0085-0
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Abstract

Invading pathogens are recognized by mammalian cells through dedicated receptors found either at the cell surface or in the cytoplasm. These receptors, like the trans-membrane Toll-like Receptors (TLR) or the cytosolic Nod-like Receptors (NLR), initiate innate immunity after recognition of molecular patterns found in bacteria or viruses, such as LPS, flagellin, or double-stranded RNA. Recognition of molecules produced only by a specific pathogen, such as a viral envelop protein or a bacterial adhesin does not appear to occur. Bacterial protein toxins, however, might compose an intermediate class. Considering the diversity of toxins in terms of structure, it is unlikely that cells respond to them via specific molecular recognition. It rather appears that different classes of toxins trigger cellular changes that are sensed by the cells as danger signals, such as changes in cellular ion composition after membrane perforation by pore-forming toxins or type III secretion systems. The signaling pathways triggered through toxin-induced cell alterations will likely play a role in modulating host responses to virulent bacteria. We will here describe the few studied cases in which detection of the toxin by the host cell was addressed. The review will include not only toxins but also bacteria effectors secreted by the bacterium in to the host cell cytoplasm.

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  • Invading pathogens are recognized by mammalian cells through receptors found either at the cell surface (e.g., TLRs) or in the cytoplasm (NLRs).

    “Invading pathogens are recognized by mammalian cells through receptors found either at the cell surface (eg, trans-membrane Toll-like Receptors; TLRs), or in the cytoplasm (Nod-like Receptors (NLRs) [36,37].”

    From LC3-Associated Phagocytosis (LAP): Connections with Host Autophagy (2012) · cites this paper as [36]

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Authors
Freche, B., Reig, N., & van der Goot, F. G.
Affiliations
École Polytechnique Fédérale de Lausanne (CH)
Venue
Seminars in Immunopathology
Publisher
Springer Science and Business Media LLC
Published
2007-09
Volume
29
Issue
3
Pages
249-260
ISSN
  • 1863-2297 (ISSN-L)
  • 1863-2300
DOI
10.1007/s00281-007-0085-0
OpenAlex
W1976759029
Cited by
52
References
2
Citations by year
2022: 1 · 2020: 3 · 2019: 2 · 2016: 1 · 2015: 3 · 2014: 9 · 2013: 3 · 2012: 7
FWCI
0.49
Type
journal article
Language
en
Open access
Licence
Locations
  • Seminars in Immunopathology (publishedVersion)
  • PubMed (publishedVersion)
  • reroDoc Digital Library (submittedVersion)
  • Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Agricultural and Biological Sciences › Plant Science › Plant-Microbe Interactions and Immunity
Keywords
inflammasome, bacterial toxins, bacterial effector proteins, innate immunity, damage-associated molecular patterns, pore-forming toxins, type III secretion system, membrane perforation, host-pathogen interaction
MeSH terms
Animals, Bacterial Infections, Bacterial Proteins, Bacterial Toxins, Enzyme Activation, Humans, Inflammation, Signal Transduction, Models, Immunological, Caspase 1, Multiprotein Complexes, Toll-Like Receptors, Nod Signaling Adaptor Proteins

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