[Show abstract][Hide abstract] ABSTRACT: Abstract Breastfeeding protects the neonate against pathogen infection. Major mechanisms of protection include human milk glycoconjugates functioning as soluble receptor mimetics that inhibit pathogen binding to the mucosal cell surface, prebiotic stimulation of gut colonization by favorable microbiota, immunomodulation, and as a substrate for bacterial fermentation products in the gut. Human milk proteins are predominantly glycosylated, and some biological functions of these human milk glycoproteins (HMGPs) have been reported. HMGPs range in size from 14 kDa to 2,000 kDa and include mucins, secretory immunoglobulin A, bile salt-stimulated lipase, lactoferrin, butyrophilin, lactadherin, leptin, and adiponectin. This review summarizes known biological roles of HMGPs that may contribute to the ability of human milk to protect neonates from disease.
Breastfeeding Medicine 05/2013; 8(4). DOI:10.1089/bfm.2013.0016 · 1.25 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background:
At the clinical onset of type 1 diabetes mellitus (T1D), enterovirus (EV) infections are suspected to play a role. EVs in blood are seen as a possible biomarker of T1D. EV infections may occur in temporal and geographic clusters and may spread within families.
We checked whether EVs were present in the blood of newly diagnosed diabetic probands and of their consenting siblings and parents. We aimed at evaluating the frequency of EV infection, whether infections were spreading within families, and which EV species were involved.
Subjects and methods:
Blood was drawn from 24 newly diagnosed diabetic children/adolescents and their family members (20 siblings and 41 parents). Blood donors and non-diabetic children/adolescents diagnosed with overweight/short stature were used as controls. RNA was extracted from plasma/leukocytes. Reverse-transcription polymerase chain reaction assays capable of detecting virtually all EV types and of giving preliminary species identification were used.
Results and conclusions:
EV genomes were found in the blood of 19 of 24 (79%) diabetics, 12 of 20 (60%) non-diabetic siblings, 26 of 41 (63%) parents, and 1 of 29 (3%) pediatric controls. EVs of the A, B, C, and D species were detected, with the B and C species more prevalent. Probands and virus-positive members of each family consistently shared the same EV species. During follow-up, 4 of 20 (20%) siblings of diabetic probands developed T1D with a latency of 3-25 months. In conclusion, infection by different EV species is highly prevalent at the clinical onset and extends to family members. EV may represent a precipitating factor of T1D. However, the disease only develops in a subset of infected individuals.
[Show abstract][Hide abstract] ABSTRACT: It is widely accepted that type 1 diabetes mellitus (T1DM) is an autoimmune disease resulting from an interaction between immunologic, genetic, and environmental factors. However, the exact mechanism leading to the development of T1DM remain incomplete. There is a large body of evidence pointing towards the important role of toll-like receptor (TLR) activation and vitamin D deficiency in T1DM pathogenesis. In this article we review the available data on the influence of TLRs’ level of activation and vitamin D status on the risk of the development of T1DM in humans and rodent models. We also summarized the current information regarding the interactions between TLRs’ level of activation, vitamin D status, and various environmental factors, such as enteroviral infections, the gut microbiota, and breastfeeding substitution, among others. Our results stipulate that vitamin D seems to protect against T1DM by reducing the TLRs’ level of activation.This article is protected by copyright. All rights reserved.
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