Gut epithelial impairment, microbial translocation and immune system activation in inflammatory bowel disease-associated spondyloarthritis.

OBJECTIVES: Gut microbiota has been widely reported to be involved in systemic inflammation through microbial translocation and T cell activation in several diseases. In this work we aimed to investigate bacterial infiltration and epithelial impairment in the gut of patients with IBD-associated SpA (SpA-IBD), as well as the relationship of microbial translocation with immune system activation and their putative role in the pathogenesis of joint inflammation in IBD patients. METHODS: Tight-junction proteins (TJPs) occludin and claudin-1/-4 and bacteria were assessed by real-time PCR analysis and immunohistochemical staining of the ileum. Intestinal fatty acid binding protein (I-FABP), lipopolysaccharides (LPS), soluble CD14 (sCD14), sclerostin and anti-sclerostin antibodies (anti-sclerostin-IgG) were assayed with ELISAs and peripheral mononuclear blood cells with flow cytometry. LPS and sCD14 were used in vitro to stimulate a human osteoblast cell line. RESULTS: Compared with IBD, ileal samples from SpA-IBD patients showed bacterial infiltration, epithelial damage and downregulation of TJPs. In sera, they showed higher serum levels of I-FABP, LPS, sCD14 (the latter correlating with sclerostin and anti-sclerostin-IgG) and higher CD80+/CD163+ and lower CD14+ mononuclear cells. In vitro experiments demonstrated that only the LPS and sCD14 synergic action downregulates sclerostin expression in osteoblast cells. CONCLUSION: SpA-IBD patients are characterized by gut epithelium impairment with consequent translocation of microbial products into the bloodstream, immune system activation and an increase of specific soluble biomarkers. These findings suggest that gut dysbiosis could be involved in the pathogenesis of SpA-IBD and it could hopefully prompt the use of these biomarkers in the follow-up and management of IBD patients.

Use of Hydrosurgical Debridement System for Silicone Gel Removal after Breast Implant Rupture.

Breast implant rupture is one of the most common complications in aesthetic and reconstructive surgery. Furthermore, this problem is closely linked to capsular contracture. It is therefore crucially important to effectively and promptly remove silicone leakage from breast pockets. Several techniques are described in the literature and have been typically used for this procedure. Hydrosurgical debridement (HD), which is usually applied in wound care to treat wounds, could be useful for the removal of the silicone leaked from prosthesis pockets after breast implant rupture. An entire periprosthetic capsule that contained a ruptured implant with silicone leakage was removed from a left breast. Half of the capsule was treated with HD, whereas the other half was left untreated as a control. Samples were processed by light microscopy and scanning electron microscopy for morphological analyses. light microscopy demonstrated that the nontreated tissues had a typical synovial-like structure with a middle layer of connective tissue in which there were numerous rounded empty spaces which contained silicone. In contrast, the superficial connective region of the treated tissues (T) had fewer and flattened spaces where the silicone was detected. Scanning electron microscopic analysis showed that in the T samples, the capsule thickness was compact compared with that of the nontreated tissues. Furthermore, the fibrous components appeared well organized with few and smaller silicone lacunae. HD is useful for the removal of silicone (ex vivo) from capsular surfaces after implant rupture. Because of its safety characteristics, this technique could be successfully used in vivo.