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

Détails

Ressource 1Télécharger: BIB_DA969040390C.P001.pdf (468.73 [Ko])
Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_DA969040390C
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Mycobacterium avium subsp. paratuberculosis in an Italian Cohort of Type 1 Diabetes Pediatric Patients.
Périodique
Clinical and Developmental Immunology
Auteur(s)
Manca Bitti M.L., Masala S., Capasso F., Rapini N., Piccinini S., Angelini F., Pierantozzi A., Lidano R., Pietrosanti S., Paccagnini D., Sechi L.A.
ISSN
1740-2530 (Electronic)
ISSN-L
1740-2522
Statut éditorial
Publié
Date de publication
2012
Volume
2012
Pages
785262
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Résumé
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.
Pubmed
Web of science
Open Access
Oui
Création de la notice
20/09/2012 19:19
Dernière modification de la notice
09/05/2019 2:05
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