We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Uncovering the relationship between macrophages and polypropylene surgical mesh
Summary
Researchers studied how polypropylene surgical mesh, commonly used to treat stress urinary incontinence, degrades inside the body when exposed to mechanical forces and oxidation. The degraded mesh surface cracked and triggered inflammatory and scarring responses in immune cells, helping explain why these implants sometimes cause serious complications. This study demonstrates that plastic materials can break down within the body and provoke harmful immune responses, which is directly relevant to concerns about microplastic accumulation in human tissues.
Currently, in vitro testing examines the cytotoxicity of biomaterials but fails to consider how materials respond to mechanical forces and the immune response to them; both are crucial for successful long-term implantation. A notable example of this failure is polypropylene mid-urethral mesh used in the treatment of stress urinary incontinence (SUI). The mesh was largely successful in abdominal hernia repair but produced significant complications when repurposed to treat SUI. Developing more physiologically relevant in vitro test models would allow more physiologically relevant data to be collected about how biomaterials will interact with the body. This study investigates the effects of mechanochemical distress (a combination of oxidation and mechanical distention) on polypropylene mesh surfaces and the effect this has on macrophage gene expression. Surface topology of the mesh was characterised using SEM and AFM; ATR-FTIR, EDX and Raman spectroscopy was applied to detect surface oxidation and structural molecular alterations. Uniaxial mechanical testing was performed to reveal any bulk mechanical changes. RT-qPCR of selected pro-fibrotic and pro-inflammatory genes was carried out on macrophages cultured on control and mechanochemically distressed PP mesh. Following exposure to mechanochemical distress the mesh surface was observed to crack and craze and helical defects were detected in the polymer backbone. Surface oxidation of the mesh was seen after macrophage attachment for 7 days. These changes in mesh surface triggered modified gene expression in macrophages. Pro-fibrotic and pro-inflammatory genes were upregulated after macrophages were cultured on mechanochemically distressed mesh, whereas the same genes were down-regulated in macrophages exposed to control mesh. This study highlights the relationship between macrophages and polypropylene surgical mesh, thus offering more insight into the fate of an implanted material than existing in vitro testing.
Sign in to start a discussion.
More Papers Like This
Characterization and quantification of oxidative stress induced particle debris from polypropylene surgical mesh
Researchers characterized and quantified particle debris released from polypropylene surgical mesh under oxidative stress conditions, raising concerns about microplastic generation from implanted medical devices and potential host tissue responses.
Influence of polypropylene mesh degradation on tissue inflammatory reaction
Polypropylene surgical mesh implants were found to degrade in vivo through surface cracking and peeling, releasing particles and altering the inflammatory tissue response around the implant. The study raises concerns about the long-term biocompatibility of polypropylene mesh given its degradation behavior.
Mitigating microplastic-induced organ Damage: Mechanistic insights from the microplastic-macrophage axes
This review is the first comprehensive examination of how microplastics interact with macrophages, the immune cells responsible for engulfing and removing foreign particles from the body. When macrophages absorb microplastics, the resulting oxidative stress disrupts their normal function, leading to inflammation and organ damage, with gut bacteria potentially playing a role in this harmful process.
Polyethylene microplastics impede the innate immune response by disrupting the extracellular matrix and signaling transduction
Mice exposed to polyethylene microplastics showed a weakened immune response when challenged with bacterial toxins, with lower levels of immune signaling molecules and reduced immune cell activity. The microplastics disrupted proteins in the extracellular matrix, the structural framework around cells in the liver and spleen, which impaired immune signaling. This suggests that microplastic accumulation in organs could make the body less effective at fighting infections.
Nanoplastics and Immunity: Investigating the Extracellular Matrix’s Influence on Macrophage Interaction with Polystyrene Nanoparticles
Researchers investigated how extracellular matrix components affect macrophage uptake of polystyrene nanoplastics, finding that the surrounding matrix modulates nanoplastic-immune cell interactions — with implications for understanding how nanoplastics evade or engage the innate immune response.