Fibronectin enhances Campylobacter fetus interaction with extracellular matrix components and INT 407 cells

Area of Science:

• Microbiology
• Pathogenesis
• Bacterial Adherence

Background:

• Campylobacter fetus is a significant pathogen in livestock and humans.
• Bacterial attachment is critical for establishing infection, but specific adhesins for C. fetus remain unidentified.
• Scanning electron microscopy indicated C. fetus adheres to the extracellular matrix (ECM) of human colon tissue.

Purpose of the Study:

• To investigate the role of the extracellular matrix (ECM) in mediating Campylobacter fetus adherence.
• To identify specific ECM components involved in C. fetus attachment.
• To elucidate the mechanism by which C. fetus interacts with host tissues.

Main Methods:

• Solid-phase binding assays were used to assess the binding of 7 C. fetus strains to immobilized ECM components.
• Ligand immunoblots were performed to identify protein interactions.
• Modified ECM binding assays and cell adherence assays with INT 407 cells were conducted.
• Inhibition assays using RGD-containing peptides were employed to investigate receptor involvement.

Main Results:

• All tested C. fetus strains demonstrated adherence to fibronectin, a key ECM component.
• The S-layer protein of C. fetus was identified as a primary binding site for fibronectin.
• Soluble fibronectin significantly enhanced the attachment of S-layer-expressing strains to other ECM components and INT 407 intestinal cells.
• Fibronectin-mediated adherence to INT 407 cells involved integrin receptors, as shown by RGD peptide inhibition.

Conclusions:

• Campylobacter fetus binds to immobilized fibronectin and utilizes soluble fibronectin to augment its attachment to other ECM proteins and intestinal epithelial cells.
• Fibronectin plays a crucial role in promoting bacterial adherence in vivo, facilitating initial interactions with mucosal and submucosal surfaces.
• Understanding this fibronectin-mediated adherence mechanism provides insights into C. fetus pathogenesis and host-pathogen interactions.