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Related Experiment Video

Updated: May 21, 2026

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues

Published on: February 19, 2019

Staphylococcus aureus surface protein SdrE binds complement regulator factor H as an immune evasion tactic.

Julia A Sharp¹, Charlene G Echague, Pamela S Hair

¹Department of Pediatrics, Eastern Virginia Medical School, Norfolk, Virginia, United States of America. sharpja@evms.edu

|June 8, 2012

Summary

Staphylococcus aureus uses surface protein SdrE to bind factor H (fH), a complement regulator. This binding inhibits the complement pathway, helping the bacteria evade immune responses.

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Area of Science:

Microbiology
Immunology
Bacterial Pathogenesis

Background:

Staphylococcus aureus, a major pathogen, employs immune evasion strategies.
Complement system regulation is crucial for host defense against bacteria.
Factor H (fH) is a key regulator of the complement alternative pathway.

Purpose of the Study:

Identify Staphylococcus aureus surface proteins that bind factor H.
Investigate the role of SdrE in factor H recruitment and complement evasion.

Main Methods:

Purified fH overlay and cross-linking with mass spectrometry to identify fH-binding proteins.
Recombinant SdrE (rSdrE) binding assays with purified fH and serum.
Functional assays using surrogate bacteria (Lactococcus lactis) expressing SdrE.

Main Results:

SdrE was identified as a novel surface protein that binds factor H (fH).
Recombinant SdrE bound fH in a time- and dose-dependent manner.
SdrE-bound fH retained cofactor activity for factor I (fI)-mediated C3b cleavage, generating iC3b.
Surface expression of SdrE on Lactococcus lactis enhanced fH recruitment and iC3b generation.
SdrE expression reduced C3 deposition, C5a generation, and polymorphonuclear cell killing.

Conclusions:

SdrE is the first identified Staphylococcus aureus surface protein that binds factor H.
SdrE-mediated factor H binding is a novel immune evasion mechanism for Staphylococcus aureus.
Targeting SdrE interaction with factor H may offer therapeutic strategies against S. aureus infections.