Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1468-1477 |
| Number of pages | 10 |
| Journal | Journal of Clinical Endocrinology and Metabolism |
| Volume | 102 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - 2017 |
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Duodenal mucosa of patients with type 1 diabetes shows distinctive inflammatory profile and microbiota. / Pellegrini, Silvia; Sordi, V; Bolla, AM; Saita, D; Ferrarese, R; Canducci, F; Clementi, M; Invernizzi, F; Mariani, A.; Bonfanti, R; Barera, G; Testoni, PA; Doglioni, C; Bosi, E; Piemonti, L.
In: Journal of Clinical Endocrinology and Metabolism, Vol. 102, No. 5, 2017, p. 1468-1477.Research output: Contribution to journal › Article
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TY - JOUR
T1 - Duodenal mucosa of patients with type 1 diabetes shows distinctive inflammatory profile and microbiota
AU - Pellegrini, Silvia
AU - Sordi, V
AU - Bolla, AM
AU - Saita, D
AU - Ferrarese, R
AU - Canducci, F
AU - Clementi, M
AU - Invernizzi, F
AU - Mariani, A.
AU - Bonfanti, R
AU - Barera, G
AU - Testoni, PA
AU - Doglioni, C
AU - Bosi, E
AU - Piemonti, L
PY - 2017
Y1 - 2017
N2 - Context: Increasing evidences suggest a correlation between gut and type 1 diabetes (T1D). Objective: The objective of this study is to evaluate the gut inflammatory profile and microbiota in patients with T1D compared with healthy control (CTRL) subjects and patients with celiac disease (CD) as gut inflammatory disease controls. Design/Setting/Participants: The inflammatory status and microbiome compositionwere evaluated in biopsies of the duodenal mucosa of patients with T1D (n = 19), in patients with CD (n = 19), and CTRL subjects (n = 16) recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. Main Outcome Measures: Inflammation was evaluated by gene expression study and immunohistochemistry. Microbiome composition was analyzed by 16S ribosomal RNA gene sequencing. Results: An increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFa, and VEGFA was observed in patientswith T1D compared with CTRL subjects and patientswith CD. Immunohistochemical analysis confirmed T1D-specific inflammatory status compared with healthy and CD control tissues, mainly characterized by the increase of the monocyte/macrophage lineage infiltration. The T1D duodenal mucosal microbiome results were different from the other groups, with an increase in Firmicutes and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes. The expression of genes specific for T1D inflammation was associated with the abundance of specific bacteria in the duodenum. Conclusions: This study shows that duodenal mucosa in T1D presents disease-specific abnormalities in the inflammatory profile and microbiota. Understanding the mechanisms underlying these features is critical to disentangle the complex pathogenesis of T1D and to gain new perspectives for future therapies targeting the intestine. (J Clin Endocrinol Metab 102: 1468-1477, 2017). © 2017 Endocrine Society.
AB - Context: Increasing evidences suggest a correlation between gut and type 1 diabetes (T1D). Objective: The objective of this study is to evaluate the gut inflammatory profile and microbiota in patients with T1D compared with healthy control (CTRL) subjects and patients with celiac disease (CD) as gut inflammatory disease controls. Design/Setting/Participants: The inflammatory status and microbiome compositionwere evaluated in biopsies of the duodenal mucosa of patients with T1D (n = 19), in patients with CD (n = 19), and CTRL subjects (n = 16) recruited at San Raffaele Scientific Institute, in Milan, Italy, between 2009 and 2015. Main Outcome Measures: Inflammation was evaluated by gene expression study and immunohistochemistry. Microbiome composition was analyzed by 16S ribosomal RNA gene sequencing. Results: An increased expression of CCL13, CCL19, CCL22, CCR2, COX2, IL4R, CD68, PTX3, TNFa, and VEGFA was observed in patientswith T1D compared with CTRL subjects and patientswith CD. Immunohistochemical analysis confirmed T1D-specific inflammatory status compared with healthy and CD control tissues, mainly characterized by the increase of the monocyte/macrophage lineage infiltration. The T1D duodenal mucosal microbiome results were different from the other groups, with an increase in Firmicutes and Firmicutes/Bacteroidetes ratio and a reduction in Proteobacteria and Bacteroidetes. The expression of genes specific for T1D inflammation was associated with the abundance of specific bacteria in the duodenum. Conclusions: This study shows that duodenal mucosa in T1D presents disease-specific abnormalities in the inflammatory profile and microbiota. Understanding the mechanisms underlying these features is critical to disentangle the complex pathogenesis of T1D and to gain new perspectives for future therapies targeting the intestine. (J Clin Endocrinol Metab 102: 1468-1477, 2017). © 2017 Endocrine Society.
U2 - 10.1210/jc.2016-3222
DO - 10.1210/jc.2016-3222
M3 - Article
VL - 102
SP - 1468
EP - 1477
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
SN - 0021-972X
IS - 5
ER -