Bacterial inhibition of inflammatory responses via TLR-independent mechanisms

Authors

  • Vladimir V. Kravchenko,

    Corresponding author
    • Department of Immunology & Microbial Science, The Scripps Research Institute, La Jolla, CA, USA
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  • Gunnar F. Kaufmann

    Corresponding author
    1. Department of Chemistry, The Scripps Research Institute, La Jolla, CA, USA
    Current affiliation:
    1. Sorrento Therapeutics, Inc., San Diego, CA, USA
    • Department of Immunology & Microbial Science, The Scripps Research Institute, La Jolla, CA, USA
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For correspondence. E-mail kaufmann@scripps.edu; Tel. (+1) 858 784 2517; Fax (+1) 858 784 2595; E-mail vkrav@scripps.edu; Tel. (+1) 858 784 9170; Fax (+1) 858 784 8239.

Summary

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.

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