Biofilm-Associated Implant Infections and Host Immune Response

Biofilm-associated implant infections arise when microbial communities adhere to the surface of prosthetic devices, producing a protective extracellular matrix that impedes antibiotic penetration and shields bacteria from immune clearance. Staphylococcus aureus and Staphylococcus epidermidis are principal culprits, although Gram-negative organisms also contribute. Upon implantation, host pattern-recognition receptors trigger innate defence cascades, recruiting neutrophils and monocytes that differentiate into macrophages. In healthy scenarios, macrophages adopt a pro-inflammatory phenotype to clear pathogens. In biofilm contexts, however, the microenvironment favours expansion of myeloid-derived suppressor cells and alternative (M2) macrophages, promoting an anti-inflammatory milieu that facilitates bacterial persistence. Chronicity of infection leads to prosthetic loosening, periprosthetic osteolysis and systemic spread. Recent studies have revealed the metabolic basis of immune suppression within biofilms, novel mechanical and pharmacological approaches to disrupt biofilms and strategies to reprogramme host immunity. Integrating antimicrobial technologies with immunomodulatory design of biomaterials offers a promising route to restore effective host defence and improve implant longevity.

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Biofilm-Associated Implant Infections and Host Immune Response publication trend

The graph below shows the total number of articles in biofilm-associated implant infections and host immune response across all publications each year (not limited to Nature Index journals).

Technical terms

Biofilm: A structured microbial community embedded in a self-produced extracellular polymeric matrix that adheres to surfaces and resists antimicrobial and immune attack.

Myeloid-derived suppressor cells (MDSCs): A heterogeneous population of immature myeloid cells that down-regulate immune responses and foster an anti-inflammatory environment during chronic infections.

Macrophage polarization: The functional differentiation of macrophages into pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes in response to microenvironmental signals.

Glycolysis–HIF1α axis: A metabolic pathway in which enhanced glycolytic flux and activation of hypoxia-inducible factor 1α drive immunosuppressive cell functions within hypoxic biofilm niches.

Immunomodulatory biomaterials: Engineered surfaces or carriers designed to interact with and direct host immune cells to enhance antimicrobial defence rather than solely relying on direct antibacterial agents.

References

1. Ultrasound‐Stimulated “Exocytosis” by Cell‐Like Microbubbles Enhances Antibacterial Species Penetration and Immune Activation Against Implant Infection. Advanced Science (2023).
2. Granulocytic myeloid-derived suppressor cell activity during biofilm infection is regulated by a glycolysis-HIF1a axis. Journal of Clinical Investigation (2024).
3. Staphylococcus aureus biofilm elicits the expansion, activation and polarization of myeloid-derived suppressor cells in vivo and in vitro. PLOS ONE (2017).
4. MyD88-Dependent Signaling Influences Fibrosis and Alternative Macrophage Activation during Staphylococcus aureus Biofilm Infection. PLOS ONE (2012).
5. Interaction Between Staphylococcal Biofilm and Bone: How Does the Presence of Biofilm Promote Prosthesis Loosening?. Frontiers in Microbiology (2019).
6. Immunomodulatory biomaterials for implant-associated infections: from conventional to advanced therapeutic strategies. Biomaterials Research (2022).