Downregulation of bactericidal peptides in enteric infections: a novel immune escape mechanism with bacterial DNA as a potential regulator.
Islam. D D; Bandholtz. L L; Nilsson. J J; Wigzell. H H; Christensson. B B; Agerberth. B B; Gudmundsson. G G
Key Findings
- LL‑37 and beta‑defensin‑1 levels are reduced early in Shigella infection
- The down‑regulation is seen in human biopsies and in epithelial/monocyte cell cultures
- Shigella plasmid DNA can mediate the suppression of these peptides
Practical Outcomes
- Understanding that infections can suppress LL‑37 suggests you might want to support innate immunity (e.g., vitamin D, gut‑friendly nutrients) during or after gut infections. Monitoring or boosting LL‑37 levels could help maintain barrier defenses, though the study doesn’t give specific dosing or protocols.
Summary
During early Shigella infection, the body lowers the production of two key antimicrobial peptides, LL‑37 and human beta‑defensin‑1, which may let the bacteria stick to and invade gut cells. The study shows this happens both in patient tissue samples and lab-grown cells, and points to Shigella plasmid DNA as a trigger.
Abstract
Antibacterial peptides are active defense components of innate immunity. Several studies confirm their importance at epithelial surfaces as immediate barrier effectors in preventing infection. Here we report that early in Shigella spp. infections, expression of the antibacterial peptides LL-37 and human beta-defensin-1 is reduced or turned off. The downregulation is detected in biopsies from patients with bacillary dysenteries and in Shigella- infected cell cultures of epithelial and monocyte origin. This downregulation of immediate defense effectors might promote bacterial adherence and invasion into host epithelium and could be an important virulence parameter. Analyses of bacterial molecules causing the downregulation indicate Shigella plasmid DNA as one mediator.
Study Information
pubmed
2001
2001-02-01T00:00:00.000Z
10.1038/84627
445
35