Bacterial inhibition of inflammatory responses via TLR-independent mechanisms.

Abstract

Identification of cellular processes modulated by microbial organisms that undermine and disarm mammalian host defences against bacterial invaders has been the focus of significant biomedical research. In this microreview we will illustrate the role of bacterial N-acyl homoserine lactones (AHL) as a strategy utilized by Gram-negative bacterial pathogens to enable colonization of the host through AHL-mediated inhibition of inflammation induced via innate immune receptor mechanisms. We will also highlight some of the signalling pathways in which the study of AHL-mediated effects on mammalian cells might lead to the discovery of global underlying principles linking inflammation and immunity to many chronic human diseases, including cancer and obesity.

• Authors: Vladimir V Kravchenko, Gunnar F Kaufmann
• Journal: Cellular microbiology (Cell Microbiol) Vol. 15 Issue 4 Pg. 527-36 (Apr 2013) ISSN: 1462-5822 [Electronic] India
• PMID: 23323541 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
• Copyright: © 2013 Blackwell Publishing Ltd.

Chemical References

• Acyl-Butyrolactones

Topics

• Acyl-Butyrolactones (metabolism)
• Bacteria (immunology, metabolism)
• Host-Pathogen Interactions (drug effects)
• Humans
• Immune Evasion
• Immunity, Innate (drug effects)
• Inflammation