Related Experiment Videos
Mapping the Prosthetic-Host Interactome: From Systemic Inflammation to Biological Integration in Mesh-Enhanced
Florentina Cristina Finascu1, Valentin Constantin Oprea2,3, Mihai Toma3
1Doctoral School of Medicine, "George Emil Palade" University of Medicine, Pharmacy, Science and Technology, 540139 Targu-Mures, Romania.
International Journal of Molecular Sciences
|July 28, 2026
Summary
Mesh-enriched therapies (METs) reprogram the host-prosthetic interaction, reducing foreign body responses (FBRs) and inflammation after hernia repair. METs promote tissue regeneration and integration, shifting hernia repair towards active biocamouflage and long-term healing.
Area of Science:
- Biomaterials Science
- Regenerative Medicine
- Surgical Innovation
Background:
- Synthetic meshes reduce hernia recurrence but cause persistent foreign body responses (FBRs).
- Mesh-enriched therapies (METs) utilize autologous cellular components to promote regenerative reprogramming of the host-prosthetic interface.
- Understanding the systemic and local host responses to synthetic meshes is crucial for improving hernia repair outcomes.
Purpose of the Study:
- To conduct a scoping review of evidence on systemic inflammation, local FBR, and bio-augmentation strategies in mesh-based hernia repair.
- To synthesize findings on the host-prosthetic interactome following implantation of synthetic meshes and METs.
- To evaluate the efficacy of METs in mitigating FBR and promoting regenerative healing.
Main Methods:
- Systematic literature search following PRISMA-ScR guidelines across PubMed, Embase, and Scopus (2000-2025).
- Utilized the PCC (Population, Concept, Context) framework for evidence mapping.
- Synthesized sixty-five studies categorized into systemic response, local FBR, and MET integration.
Main Results:
- A 'foreign body signature' with C-reactive protein (CRP) and interleukin-6 (IL-6) spikes within 48h post-implantation was identified.
- Long-term explant data (up to 180 months) showed perpetual immune-mediated FBR driven by MMP-2 remodeling and 'bridging fibrosis'.
- METs shifted macrophage phenotypes towards pro-regenerative profiles, enhanced angiogenesis (VEGF), and optimized collagen ratios, but precise TGF-β1 dosing is critical to prevent hyper-fibrosis.
Conclusions:
- METs transform hernia repair from mechanical reinforcement to active biocamouflage and integration.
- By modulating the immune response (Th1/Th2 rheostat), METs mitigate chronic inflammation and complications.
- Standardized clinical trials are necessary to optimize METs for hybrid integration and therapeutic window.
Related Concept Videos
01:12Chronic Inflammation: Introduction
Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
02:17The Tumor Microenvironment
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...