Document Detail


Differential regulation of caspase-1 activation via NLRP3/NLRC4 inflammasomes mediated by aerolysin and type III secretion system during Aeromonas veronii infection.
MedLine Citation:
PMID:  21037094     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Aeromonas spp. are Gram-negative bacteria that cause serious infectious disease in humans. Such bacteria have been shown to induce apoptosis in infected macrophages, yet the host responses triggered by macrophage death are largely unknown. In this study, we demonstrate that the infection of mouse bone marrow-derived macrophages with Aeromonas veronii biotype sobria triggers activation of caspase-1 with the ensuing release of IL-1β and pyroptosis. Caspase-1 activation in response to A. veronii infection requires the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain and both the NLRP3 and NLRC4 inflammasomes. Furthermore, caspase-1 activation requires aerolysin and a functional type III secretion system in A. veronii. Aerolysin-inducing caspase-1 activation is mediated through the NLRP3 inflammasome, with aerolysin-mediated cell death being largely dependent on the NLRP3 inflammasome. In contrast, the type III secretion system activates both the NLRP3 and NLRC4 inflammasomes. Inflammasome-mediated caspase-1 activation is also involved in host defenses against systemic A. veronii infection in mice. Our results indicated that multiple factors from both the bacteria and the host play a role in eliciting caspase-1 activation during A. veronii infection.
Authors:
Andrea J McCoy; Yukiko Koizumi; Naomi Higa; Toshihiko Suzuki
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-10-29
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-11-18     Completed Date:  2011-01-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  7077-84     Citation Subset:  AIM; IM    
Affiliation:
Department of Molecular Bacteriology and Immunology, Graduate School of Medicine, University of the Ryukyus, Nishiharacho, Okinawa, Japan.
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MeSH Terms
Descriptor/Qualifier:
Aeromonas / immunology*,  pathogenicity
Animals
Apoptosis Regulatory Proteins / deficiency,  genetics,  physiology*
Bacterial Secretion Systems / immunology*
Bacterial Toxins / biosynthesis
Bone Marrow Cells / immunology,  microbiology,  pathology
Calcium-Binding Proteins / deficiency,  genetics,  physiology*
Carrier Proteins / genetics,  physiology*
Caspase 1 / deficiency,  genetics,  metabolism*
Cell Death / genetics,  immunology
Cells, Cultured
Gram-Negative Bacterial Infections / enzymology,  genetics,  immunology
Inflammasomes / deficiency,  genetics,  physiology*
Macrophages / immunology,  microbiology,  pathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Pore Forming Cytotoxic Proteins / biosynthesis,  physiology*
Chemical
Reg. No./Substance:
0/Apoptosis Regulatory Proteins; 0/Bacterial Toxins; 0/CIAS1 protein, mouse; 0/Calcium-Binding Proteins; 0/Carrier Proteins; 0/Inflammasomes; 0/Ipaf protein, mouse; 0/Pore Forming Cytotoxic Proteins; 53126-24-2/aerolysin; EC 3.4.22.36/Caspase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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