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Invasion of Human Cells by a Bacterial Pathogen

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Published on: March 21, 2011

Group A Streptococcus tissue invasion by CD44-mediated cell signalling.

C Cywes¹, M R Wessels

¹Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

|December 12, 2001

Summary

Streptococcus pyogenes uses its hyaluronic acid capsule to mimic host molecules, triggering cell shape changes and invasion. This interaction with CD44 on epithelial cells facilitates bacterial entry through paracellular routes.

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Area of Science:

Microbiology
Cell Biology
Pathogenesis

Background:

Streptococcus pyogenes (group A Streptococcus, GAS) causes pharyngeal and skin infections.
GAS utilizes its hyaluronic acid capsule to bind to the CD44 receptor on human epithelial cells.
This binding interaction is crucial for bacterial adhesion and subsequent host cell manipulation.

Purpose of the Study:

To investigate if the GAS hyaluronic acid capsule's molecular mimicry of CD44 induces cellular responses.
To elucidate the mechanisms by which GAS invades host tissues.

Main Methods:

Studied CD44-dependent GAS binding to human keratinocyte monolayers.
Analyzed cytoskeletal rearrangements, intercellular junction disruption, and signal transduction pathways (Rac1, ezrin, tyrosine phosphorylation).
Examined bacterial translocation in human skin models.

Main Results:

GAS binding to CD44 induced significant keratinocyte cytoskeletal changes, including membrane ruffling.
Intercellular junctions were disrupted, facilitating bacterial passage.
Signal transduction involving Rac1, ezrin, and tyrosine phosphorylation mediated these cellular responses.
GAS translocation through human skin models occurred via a paracellular route, enabled by CD44-mediated signaling.

Conclusions:

GAS manipulates host cell cytoskeleton via CD44-mediated molecular mimicry.
This mechanism promotes bacterial tissue invasion through paracellular pathways.
The findings provide a model for host cytoskeleton manipulation and invasion by extracellular pathogens.