Comment on: Immunological insights into hernia mesh implant

Correspondence to: Antonio Manenti (email: antonio.manenti_2024@libero.it)

Polyclinic Hospital

v. Del Pozzo

41124 Modena

Italy

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BJS,https://doi.org/10.1093/bjs/znag025, published 07 May 2026

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The incidence of autoimmune reaction after hernia repair performed with a polypropylene mesh implant, as precisely studied by MJCAM Gielen et al.¹ deserves further investigation from a pathophysiological perspective2. First of all, two similar conditions must be excluded, such as a pre-existing autoimmune disease, recurring during the postoperative immune depression, and a temporary postoperative inflammatory reaction triggered by abnormal molecules, such as glycoproteins and other pro-inflammatory interleukins. They derive from necro-apoptotic cells, can recruit circulating B- and T- lymphocytes and activate intra-tissue myeloid cells, such as macrophages, dendritic cells, infiltrating monocytes and granulocytes.  This pathology has to be considered a 'post-implantation syndrome', more common after vascular endografting and often characterized by a long-term recurrent mild fever, rather than a 'de novo' onset immunological disease, given its spontaneous recovery and absence of specific laboratory markers.3  Providentially, it often goes back to a more physiological and definitive 'structural immunity', whose basal architectural elements are represented by fibroblasts, derived from mesenchymal stromal cells, and capable of generating mature extracellular matrix and collagen fibrils.4 This requires a well-balanced relationship between pro- and anti-inflammatory interleukins, otherwise it can be complicated by an 'Autoimmune/autoinflammatory Syndrome Induced by Adjuvants', often favored, besides a genetic predisposition, by an insufficient population of Treg lymphocytes.4 In conclusion, the onset of a typical immunological disease cannot be simply attributed to an implanted mesh, whose fabric consists of a fine network of polypropylene threads, capable of accommodating the growing reparative tissue, in turn requiring patients' normal metabolic conditions and the absence of a proper infectious-inflammatory state.  Differently, in the case of 'meshoma' or 'plugoma', incorrect mesh positioning, displacement or bending impede any physiological contact, growth and incorporation of fibroblasts and other reparative cells, and predispose to infections, manifesting with acute symptoms. Today, they are easily identified through radiological tools.