Loading
Life sciences · Journal article
Barrier Immunity · September 16, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
ABSTRACT Neonatal dysbiosis of the gut microbiota represents a critical environmental factor promoting obesity, but the underlying immunological mechanisms remain unknown. We show here that neonatal treatment of mice with broad‐spectrum antibiotics for the first 3 weeks of life (NeoATB) resulted in the development of obesity and metabolic abnormalities in adulthood. The NeoATB mice exhibited a permanent dysbiosis of gut microbiota, decreased CD4 + Foxp3 + regulatory T cells (Tregs), and increased proinflammatory Th1 cells in visceral adipose tissue (VAT). Mechanistically, neonatal antibiotic treatment resulted in increased intestinal permeability that allowed bacterial translocation into the VAT and liver and an increase in systemic LPS levels. Consequently, VAT CD11c + MHCII + cells were activated via the TLR4 pathway to increase IL‐12‐triggered Th1‐inflammation. Moreover, the decrease in VAT Tregs in NeoATB mice was attributed to reduced infiltration of Tregs from the periphery, decreased expansion of adipose IL‐33‐mediated ST2 + Tregs, and reduced conversion of local Tregs from VAT CD4 + CD25 − Foxp3 − T cells. Thus, we have revealed a previously unrecognized immunological link between neonatal microbiota dysbiosis and the development of obesity.