Editor: Neil Fairweather
How microorganisms avoid phagocyte attraction
Article first published online: 11 DEC 2009
© 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Microbiology Reviews
Volume 34, Issue 3, pages 395–414, May 2010
How to Cite
Bestebroer, J., De Haas, C. J.C. and Van Strijp, J. A.G. (2010), How microorganisms avoid phagocyte attraction. FEMS Microbiology Reviews, 34: 395–414. doi: 10.1111/j.1574-6976.2009.00202.x
- Issue published online: 1 APR 2010
- Article first published online: 11 DEC 2009
- Received 3 March 2009; revised 29 November 2009; accepted 30 November 2009.Final version published online 4 January 2010.
- immune evasion;
Microorganisms have developed several mechanisms to modulate the host immune system to increase their survival and propagation in the host. Their presence in the host is not only revealed by self-produced peptides but also through host-derived chemokines and active complement fragments. These so-called chemoattractants are recognized by G protein-coupled receptors (GPCRs) expressed on leukocyte cell membranes. Activation of GPCRs triggers leukocyte activation and guides their recruitment to the site of infection. Therefore, GPCRs play a central role in leukocyte trafficking leading to microbial clearance. It is therefore not surprising that microorganisms are able to sabotage this arm of the immune response. Different microorganisms have evolved a variety of tactics to modulate GPCR activation. Here, we review the mechanisms and proteins used by major human pathogens and less virulent microorganisms that affect GPCR signaling. While viruses generally produce receptor and chemoattractant mimics, parasites and bacteria such as Staphylococcus aureus, Streptococcus pyogenes, Porphyromonas gingivalis, and Bordetella pertussis secrete proteins that affect receptor signaling, directly antagonize receptors, cleave stimuli, and even prevent stimulus generation. As the large arsenal of GPCR modulators aids prolonged microbial persistence in the host, their study provides us a better understanding of microbial pathogenesis.