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Buller, S.

Publications and source records attributed to Buller, S..

3 recordsLinked to original sources

Immunorecognition of Streptococcus mutans secreted proteins protects against caries by limiting tooth adhesion

Childhood caries, a chronic disease affecting 60-90% of children in industrialized countries, results in lesions in primary and permanent dentition, leading to hospitalizations, emergency room visits, high treatment costs, and loss of school days. It diminishes the childs ability to learn and increases the risk of caries in adulthood. Despite multiple risk factors for caries, significant interpersonal variability unaccounted for by these factors exists. The immune system generates a personal antibody repertoire that helps maintain a balanced and healthy oral microbiome. Streptococcus mutans is a key bacterium in caries development. Utilizing mass-spectrometry, we examined which S. mutans proteins are identified by antibodies of children with and without caries and identified a core set of proteins recognizable by the immune system of most individuals. This set was enriched with proteins enabling bacterial adhesion. To study the physiological relevance of these findings, we tested the ability of saliva to prevent S. mutans adherence to tooth surfaces. Saliva from caries-free individuals, but not children with caries, was found to hinder the binding of S. mutans to teeth. These findings delineate the S. mutans proteome targeted by the immune system and suggest that the inhibition of bacterial adherence to teeth is a primary mechanism employed by the immune system to maintain oral balance and prevent caries formation. These discoveries offer fresh insights into the immune systems role in preserving oral health and preventing caries development. Targeting S. mutans proteins implicated in bacterial adhesion could be a promising strategy for preventing childhood caries.

microbiology↗

Median eminence myelin continuously turns over in adult mice

ObjectiveOligodendrocyte progenitor cell differentiation is regulated by nutritional signals in the adult median eminence (ME), but the consequences on local myelination are unknown. The aim of this study was to characterise myelin plasticity in the ME of adult mice in health or in response to chronic nutritional challenge. MethodsWe assessed new oligodendrocyte and myelin generation and stability in the ME of healthy adult male mice using bromodeoxyuridine labelling and genetic fate mapping tools. We assessed the contribution of microglia to ME myelin plasticity in PLX5622-treated C57BL6/J mice and in Pdgfra-Cre/ERT2;R26R-eYFP;Myrffl/fl mice, where adult oligodendrogenesis is genetically blunted. Finally, we investigated how 45% high fat diet or 70% caloric restriction feeding paradigms impact ME oligodendrocyte lineage progression and myelination in C57BL6/J mice. ResultsWe show that myelinating oligodendrocytes (OLs) are continuously and rapidly generated in the adult ME. Paradoxically, OL number and myelin amounts remain remarkably stable in the adult ME. In fact, the high rate of new OL and myelin generation in the ME is offset by continuous turnover of both. We show that microglia are required for continuous OL and myelin production, and that ME myelin plasticity regulates the recruitment of local immune cells. Finally, we provide evidence that ME myelination is regulated by the bodys energetic status, decreased in calorie-restricted animals, and increased in mice fed a high fat diet. ConclusionsThis study uncovers a previously unappreciated form of ME structural plasticity and mechanism of myelin remodeling in the adult brain.

neuroscience↗

Nutritional signals rapidly activate oligodendrocyte differentiation in the adult hypothalamic median eminence

The mediobasal hypothalamus (arcuate nucleus - ARC - and median eminence - ME -) controls energy balance, growth and fertility through its ability to integrate neuronal, nutritional and hormonal signals and coordinate the behavioural, neuroendocrine and metabolic responses required for these functions. While our understanding of the neural circuits downstream from ARC neurons is rapidly progressing, little is known about the function of other cell types. Here we describe an unexpected role for oligodendrocytes (OL) of the ME in monitoring nutritional signals. We show that refeeding following an overnight fast rapidly activates oligodendrocyte differentiation and the production of new OL in the ME specifically. No changes in myelination were measured in this time-frame. However, refeeding changed the expression of OL-derived extracellular matrix proteins decorin and tenascin-R, with consistent changes in the density of local perineuronal nets. Last, we show that OLs use mTORC1 signalling, a pathway required for OL differentiation, to survey energy and protein availability, specifically in the ME. We conclude that new oligodendrocytes formed in the ME in response to nutritional signals control the access of circulating metabolic cues to ARC interoceptive neurons.

neuroscience↗