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

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 I...

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Published inClinical & developmental immunology Vol. 2012; no. 2012; pp. 1 - 5
Main Authors Manca Bitti, Maria Luisa, Masala, Speranza, Capasso, Francesca, Rapini, Novella, Piccinini, Simona, Angelini, Federica, Pierantozzi, Andrea, Lidano, Roberta, Pietrosanti, Silvia, Paccagnini, Daniela, Sechi, Leonardo Antonio
Format Journal Article
LanguageEnglish
Published Cairo, Egypt Hindawi Puplishing Corporation 01.01.2012
Hindawi Publishing Corporation
John Wiley & Sons, Inc
Wiley
Subjects
Antibiotics
Antibodies
Antibodies, Bacterial - blood
Child
Clinical Study
Colleges & universities
Dairy products
Deoxyribonucleic acid
Diabetes
Diabetes mellitus
Diabetes Mellitus, Type 1 - complications
Diabetes Mellitus, Type 1 - immunology
Diabetes Mellitus, Type 1 - microbiology
Disease
DNA
DQA1 protein
Enzyme-linked immunosorbent assay
Health care
Heparin
Histocompatibility antigen HLA
Hospitals
Humans
Hypotheses
Immune response
Immunology
Infection
Infections
Islets of Langerhans
Italy
Microbiology
Mycobacterium avium
Mycobacterium avium subsp. paratuberculosis - genetics
Mycobacterium avium subsp. paratuberculosis - immunology
Mycobacterium avium subsp. paratuberculosis - isolation & purification
Mycobacterium Infections - complications
Mycobacterium Infections - microbiology
Pancreas
Paratuberculosis
Pathogenesis
Pediatrics
Polymerase chain reaction
Proteins
Risk Factors
Ruminantia
Italy
Online AccessGet full text

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Abstract 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.
AbstractList 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.
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.
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.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.
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.
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 beta -cells.
Author Paccagnini, Daniela
Masala, Speranza
Capasso, Francesca
Pierantozzi, Andrea
Angelini, Federica
Piccinini, Simona
Rapini, Novella
Sechi, Leonardo Antonio
Manca Bitti, Maria Luisa
Lidano, Roberta
Pietrosanti, Silvia
AuthorAffiliation 5 Unité d'Immuno-Allergologie et Rhumatologie, Département Médico-Chirurgical de Pédiatrie, Centre Hospitalier Universitaire Vaudois (CHUV), Rue du Bugnon 21, 1011 Lausanne, Switzerland
1 Pediatric Diabetology Unit, Policlinico di Tor Vergata, University of Rome Tor Vergata, 00133 Rome, Italy
4 Division of Pediatrics, Department of Public Health and Cell Biology, University of Rome Tor Vergata, 00165 Rome, Italy
6 Department of Internal Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
3 Department of Pediatrics, University of Rome Tor Vergata, Children's Hospital Bambino Gesù, Piazza Sant'Onofrio 4, Rome, Italy
2 Dipartimento di Scienze Biomediche, Università di Sassari, 07100 Sassari, Italy
AuthorAffiliation_xml – name: 3 Department of Pediatrics, University of Rome Tor Vergata, Children's Hospital Bambino Gesù, Piazza Sant'Onofrio 4, Rome, Italy
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– name: 2 Dipartimento di Scienze Biomediche, Università di Sassari, 07100 Sassari, Italy
– name: 4 Division of Pediatrics, Department of Public Health and Cell Biology, University of Rome Tor Vergata, 00165 Rome, Italy
– name: 6 Department of Internal Medicine, University of Rome Tor Vergata, 00133 Rome, Italy
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/22844325$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Contributor Paccagnini, Daniela
Masala, Speranza
Capasso, Francesca
Pierantozzi, Andrea
Angelini, Federica
Piccinini, Simona
Rapini, Novella
Sechi, Leonardo Antonio
Manca Bitti, Maria Luisa
Lidano, Roberta
Pietrosanti, Silvia
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Copyright Copyright © 2012 Maria Luisa Manca Bitti et al.
Copyright © 2012 Maria Luisa Manca Bitti et al. 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.
Copyright © 2012 Maria Luisa Manca Bitti et al. 2012
Copyright_xml – notice: Copyright © 2012 Maria Luisa Manca Bitti et al.
– notice: Copyright © 2012 Maria Luisa Manca Bitti et al. 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.
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Snippet Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of Johne’s disease in ruminants. Recent studies have linked MAP to type 1 diabetes...
Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of Johne’s disease in ruminants. Recent studies have linked MAP to type 1 diabetes...
Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of Johne's disease in ruminants. Recent studies have linked MAP to type 1 diabetes...
Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of Johne's disease in ruminants. Recent studies have linked MAP to type 1 diabetes...
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StartPage 1
SubjectTerms Antibiotics
Antibodies
Antibodies, Bacterial - blood
Child
Clinical Study
Colleges & universities
Dairy products
Deoxyribonucleic acid
Diabetes
Diabetes mellitus
Diabetes Mellitus, Type 1 - complications
Diabetes Mellitus, Type 1 - immunology
Diabetes Mellitus, Type 1 - microbiology
Disease
DNA
DQA1 protein
Enzyme-linked immunosorbent assay
Health care
Heparin
Histocompatibility antigen HLA
Hospitals
Humans
Hypotheses
Immune response
Immunology
Infection
Infections
Islets of Langerhans
Italy
Microbiology
Mycobacterium avium
Mycobacterium avium subsp. paratuberculosis - genetics
Mycobacterium avium subsp. paratuberculosis - immunology
Mycobacterium avium subsp. paratuberculosis - isolation & purification
Mycobacterium Infections - complications
Mycobacterium Infections - microbiology
Pancreas
Paratuberculosis
Pathogenesis
Pediatrics
Polymerase chain reaction
Proteins
Risk Factors
Ruminantia
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Title Mycobacterium avium subsp. paratuberculosis in an Italian Cohort of Type 1 Diabetes Pediatric Patients
URI https://search.emarefa.net/detail/BIM-497903
https://dx.doi.org/10.1155/2012/785262
https://www.ncbi.nlm.nih.gov/pubmed/22844325
https://www.proquest.com/docview/1038409176
https://www.proquest.com/docview/1030348565
https://www.proquest.com/docview/1221138666
https://pubmed.ncbi.nlm.nih.gov/PMC3400352
https://doaj.org/article/36e66d6b3a604f4da898fc6a39e21994
Volume 2012
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