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Clinical and Developmental Immunology
Volume 2012, Article ID 785262, 5 pages
Clinical Study

Mycobacterium avium subsp. paratuberculosis in an Italian Cohort of Type 1 Diabetes Pediatric Patients

1Pediatric Diabetology Unit, Policlinico di Tor Vergata, University of Rome Tor Vergata, 00133 Rome, Italy
2Dipartimento di Scienze Biomediche, Università di Sassari, 07100 Sassari, Italy
3Department of Pediatrics, University of Rome Tor Vergata, Children's Hospital Bambino Gesù, Piazza Sant’Onofrio 4, Rome, Italy
4Division of Pediatrics, Department of Public Health and Cell Biology, University of Rome Tor Vergata, 00165 Rome, Italy
5Unité d'Immuno-Allergologie et Rhumatologie, Département Médico-Chirurgical de Pédiatrie, Centre Hospitalier Universitaire Vaudois (CHUV), Rue du Bugnon 21, 1011 Lausanne, Switzerland
6Department of Internal Medicine, University of Rome Tor Vergata, 00133 Rome, Italy

Received 2 April 2012; Accepted 23 May 2012

Academic Editor: Luigina Romani

Copyright © 2012 Maria Luisa Manca Bitti et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of Johne’s disease in ruminants. Recent studies have linked MAP to type 1 diabetes (T1D) in the Sardinian population. The aim of this study was to investigate the prevalence of MAP infection in a T1D cohort from continental Italy compared with healthy control subjects. 247 T1D subjects and 110 healthy controls were tested for the presence of MAP. MAP DNA was detected using IS900-specific polymerase chain reaction (PCR). The presence of antibodies towards a MAP antigen, heparin binding hemoagglutinin (HBHA), was detected by ELISA. We demonstrated a higher MAP DNA prevalence in plasma samples from T1D patients and a stronger immune response towards MAP HBHA, compared with healthy control subjects. Moreover, in the recent onset patients, we observed an association between anti-MAP antibodies and HLA DQ2 (DQA1 0201/DQB1 0202). These findings taken together support the hypothesis of MAP as an environmental risk factor for the development of T1D in genetically predisposed subjects, probably involving a mechanism of molecular mimicry between MAP antigens and pancreatic islet β-cells.