Pore-forming bacterial toxins and antimicrobial peptides as modulators of ADAM function

Membrane-perturbating proteins and peptides are widespread agents in biology. Pore-forming bacterial toxins represent major virulence factors of pathogenic microorganisms. Membrane-damaging peptides constitute important antimicrobial effectors of innate immunity. Membrane perturbation can incur mult...

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Bibliographic Details
Published in:Medical microbiology and immunology 2012-11, Vol.201 (4), p.419-426
Main Authors: Reiss, Karina, Bhakdi, Sucharit
Format: Article
Language:English
Subjects:
Antimicrobial agents
Antimicrobial Cationic Peptides - metabolism
Bacteria
Bacterial Toxins - metabolism
Bacteriology
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Cell Adhesion
Cell adhesion & migration
Cell Movement
Cell Proliferation
Fundamental and applied biological sciences. Psychology
Host-Pathogen Interactions
Immunology
Matrix Metalloproteinases, Membrane-Associated - metabolism
Medical Microbiology
Microbiology
Miscellaneous
Peptides
Proteases
Review
Toxins
Virology
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Summary:Membrane-perturbating proteins and peptides are widespread agents in biology. Pore-forming bacterial toxins represent major virulence factors of pathogenic microorganisms. Membrane-damaging peptides constitute important antimicrobial effectors of innate immunity. Membrane perturbation can incur multiple responses in mammalian cells. The present discussion will focus on the interplay between membrane-damaging agents and the function of cell-bound metalloproteinases of the ADAM family. These transmembrane enzymes have emerged as the major proteinase family that mediate the proteolytic release of membrane-associated proteins, a process designated as “shedding”. They liberate a large spectrum of functionally active molecules including inflammatory cytokines, growth factor receptors and cell adhesion molecules, thereby regulating such vital cellular functions as cell–cell adhesion, cell proliferation and cell migration. ADAM activation may constitute part of the cellular recovery machinery on the one hand, but likely also promotes inflammatory processes on the other. The mechanisms underlying ADAM activation and the functional consequences thereof are currently the subject of intensive research. Attention here is drawn to the possible involvement of purinergic receptors and ceramide generation in the context of ADAM activation following membrane perturbation by membrane-active agents.
ISSN:0300-8584
1432-1831
DOI:10.1007/s00430-012-0260-3