Reply to ‘Polypropylene mesh degradation and systemic disease: biological plausibility is not clinical evidence’

We thank Chughtai, Polo and Goldman for their thoughtful commentary on our Clinical Outlook (Farr, N. T. H., Achenbach, P. & Sievert, K.-D. Effects of degradation-associated polypropylene particles in the surrounding tissue after surgical mesh implantation. Nat. Rev. Urol. 22, 791–793; 2025)1, which is important (Chughtai, B., Polo, J. & Goldman, H. B. Polypropylene mesh degradation and systemic disease: biological plausibility is not clinical evidence. Nat. Rev. Urol. https://doi.org/10.1038/s41585-026-01158-3; 2026)2. We fully agree that distinguishing biological plausibility from clinically validated causality is essential for maintaining evidence-based practice and appropriate patient counselling. However, the intent of our original article might have been misunderstood.

Our original article1 highlights emerging mechanistic evidence, including the in vivo identification of degradation-associated polypropylene nanoparticles and microparticles within surrounding tissues, and how these findings might relate to established immunological processes. As discussed in our original article and recent commentary1,3, polypropylene is not biologically inert over time. Oxidative degradation, surface modification, additive release and particle detachment are well-characterized phenomena that could alter host–material interactions4,5. These processes are likely to influence immune responses through mechanisms including macrophage activation, cytokine signalling, protein adsorption and denaturation, and the potential formation of neoantigens. In addition, broader immunological frameworks proposed in the autoimmune/inflammatory syndrome induced by adjuvants (ASIA) literature describe chronic activation of innate and adaptive immune pathways6, including associations with dysautonomia and small fibre neuropathy and reports of altered levels of autoantibodies directed against G protein-coupled receptors in some symptomatic patients. These hypotheses suggest plausible immune-mediated mechanisms that warrant prospective investigation in patients with polypropylene mesh implants. Similar interactions have also been described in a growing body of literature on the systemic effects of microplastic exposure7.

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