How microorganisms avoid phagocyte attraction

Jovanka Bestebroer*, Carla J C De Haas, Jos A G Van Strijp

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

28 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)395-414
Number of pages20
JournalFEMS Microbiology Reviews
Volume34
Issue number3
DOIs
Publication statusPublished - 1 May 2010

Keywords

  • Chemoattractants
  • Chemokines
  • Complement
  • GPCR
  • Immune evasion

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