Display Settings:

Format

Send to:

Choose Destination
Glycobiology. 2012 Aug;22(8):1019-30. doi: 10.1093/glycob/cws070. Epub 2012 Apr 5.

Infection, inflammation and host carbohydrates: a Glyco-Evasion Hypothesis.

Author information

  • 1Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.

Abstract

Microbial immune evasion can be achieved through the expression, or mimicry, of host-like carbohydrates on the microbial cell surface to hide from detection. However, disparate reports collectively suggest that evasion could also be accomplished through the modulation of the host glycosylation pathways, a mechanism that we call the "Glyco-Evasion Hypothesis". Here, we will summarize the evidence in support of this paradigm by reviewing three separate bodies of work present in the literature. We review how infection and inflammation can lead to host glycosylation changes, how host glycosylation changes can increase susceptibility to infection and inflammation and how glycosylation impacts molecular and cellular function. Then, using these data as a foundation, we propose a unifying hypothesis in which microbial products can hijack host glycosylation to manipulate the immune response to the advantage of the pathogen. This model reveals areas of research that we believe could significantly improve our fight against infectious disease.

PMID:
22492234
[PubMed - indexed for MEDLINE]
PMCID:
PMC3382345
Free PMC Article

Images from this publication.See all images (4)Free text

Fig. 1.
Fig. 2.
Fig. 3.
Fig. 4.
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Write to the Help Desk