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LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 3
2021 pubmed 14 citations

Exposure to Moderate Glycosuria Induces Virulence of Group B Streptococcus.

John. Preeti P PP; Baker. Brady C BC; Paudel. Santosh S; Nassour. Lauren L; Cagle. Hayden H; Kulkarni. Ritwij R

Key Findings

  • Moderate glycosuria (≈300 mg/dL glucose in urine) significantly boosts GBS growth and kidney bacterial load in mice.
  • Glycosuria enhances GBS adherence to bladder cells and resistance to the antimicrobial peptide LL‑37 via up‑regulation of the dltA gene.
  • Exposure to glucose increases expression of GBS virulence genes, including fimbrial (PI2a) and toxin‑producing genes.

Practical Outcomes

  • Maintain normal blood glucose levels and avoid persistent glycosuria to lower the risk of aggressive urinary infections. Monitoring urine glucose, especially for diabetics or high‑sugar diets, can be a simple preventive step. No direct LL‑37 supplementation guidance emerges from this work.

Summary

The study shows that having moderate sugar in your urine (like what can happen with high blood sugar) makes a common bacteria, Group B Strep, grow faster and become more aggressive, increasing the chance of a urinary tract infection. It also makes the bacteria better at resisting the body’s natural antimicrobial peptide LL‑37. For people interested in health optimization, this suggests that keeping blood sugar and urine glucose low could help reduce infection risk.

Abstract

To explore whether glycosuria induces virulence of uropathogens, in turn facilitating urinary tract infection (UTI), we exposed group B Streptococcus (GBS) strain 10/84 to human urine plain or with 300 mg/dL glucose (mimicking moderate glycosuria). Exposure to moderate glycosuria significantly augmented bacterial growth, kidney bacterial burden in a mouse model of ascending UTI, and virulence characteristics and expression of corresponding genes. Exposure to glycosuria increased GBS adherence to human bladder epithelial cell line and expression of corresponding PI2a fimbrial gene, antimicrobial peptide LL-37 resistance and bacterial surface charge modulating dltA, and GBS hemolytic ability and expression of genes encoding pore-forming toxins.

Study Information

Provider

pubmed

Year

2021

Date

2021-03-03T00:00:00.000Z

DOI

10.1093/infdis/jiaa443

Citations

14

References

15