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Expression of Transglutaminase in Foreskin of Children with Balanitis Xerotica Obliterans
Authors:Tiziana Russo  Monica Currò   Anna Barbera  Daniela Caccamo  Pietro Antonuccio  Salvatore Arena  Angela Simona Montalto  Saveria Parisi  Lucia Marseglia  Eloisa Gitto  Riccardo Ientile  Pietro Impellizzeri  Carmelo Romeo
Affiliation:1Department of Human Pathology of Adult and Childhood “Gaetano Barresi”, University of Messina, Messina 98125, Italy; (T.R.); (P.A.); (S.A.); (A.S.M.); (S.P.); (L.M.); (E.G.); (C.R.);2Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina 98125, Italy; (M.C.); (A.B.); (D.C.); (R.I.)
Abstract:Balanitis xerotica obliterans (BXO) is a chronic inflammatory skin disorder of unclear etiology. The etiology and the exact molecular mechanisms underlying the disease are still unknown. The human transglutaminase (TG) family consists of several proteins with catalytic activity essential for biological processes. In the present research we investigated the transcript levels of three TGs in patients operated on for congenital phimosis without or with histologically confirmed BXO; Thirty children with acquired phimosis were enrolled. The removed foreskins were sent both for histological diagnosis and for quantitative real-time PCR to evaluate the transcript levels of keratinocyte (TG1), tissue (TG2), and epidermal (TG3) transglutaminase; We observed a decrease in TG1 and TG3 transcripts by about 70% (p < 0.001) in foreskins from patients with BXO (n = 15) in comparison with patients without BXO (n = 15) and an increase in TG2 mRNA levels by 2.9 folds (p < 0.001); Reduced expression of both TG1 and TG3 was associated with the altered structure of the foreskin in BXO and can be a consequence of damage to keratinocytes. Increased expression of TG2 can be the result of chronic inflammation. TG2 overexpression can play a pivotal role in triggering and maintaining the inflammatory response in BXO patients.
Keywords:balanitis xerotica obliterans, phimosis, foreskin, transglutaminase, IFN-γ  , E-cadherin
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