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LL-37

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

Quick Stats
Studies 2230
Trials 95
Score 2
2015 pubmed 55 citations

Antimicrobial peptide Cathelicidin-BF prevents intestinal barrier dysfunction in a mouse model of endotoxemia.

Song. Deguang D; Zong. Xin X; Zhang. Haiwen H; Wang. Tenghao T; Yi. Hongbo H; Luan. Chao C; Wang. Yizhen Y

Key Findings

  • C‑BF pretreatment reduced intestinal damage and leak after LPS exposure
  • It preserved tight‑junction proteins and prevented cell death in the gut
  • It lowered TNF‑α production by blocking NF‑κB signaling in immune cells

Practical Outcomes

  • The results are promising but only in a mouse model, so there’s no direct protocol for humans yet. Biohackers should view this as early‑stage evidence that cathelicidin‑type peptides might help protect gut health during severe inflammation, but more research and safety testing are needed before any supplementation.

Summary

In mice, a snake‑venom peptide called cathelicidin‑BF given before a bacterial toxin protected the gut lining, kept the barrier tight, and lowered inflammation.

Abstract

Intestinal barrier functions are altered during the development of sepsis. Cathelicidin antimicrobial peptides, such as LL-37 and mCRAMP, can protect animals against intestinal barrier dysfunction. Cathelicidin-BF (C-BF), a new cathelicidin peptide purified from the venom of the snake Bungarus fasciatus, has been shown to have both antimicrobial and anti-inflammatory properties. This study investigated whether C-BF pretreatment could protect the intestinal barrier against dysfunction in a mouse model of endotoxemia, induced by intraperitoneal injection of LPS (10mg/kg). Mice were treated with low or high dose C-BF before treatment with LPS, and samples were collected 5h after LPS treatment. C-BF reduced LPS induced intestinal histological damage and gut permeability to 4 KD Fluorescein-isothiocyanate-conjugated dextran. Pretreatment with C-BF prevented LPS induced intestinal tight junction disruption and epithelial cell apoptosis. Moreover, C-BF down regulated the expression and secretion of TNF-α, a process involving the NF-κB signaling pathway. C-BF also reduced LPS induced TNF-α expression through the NF-κB signaling pathway in mouse RAW 264.7 macrophages. These findings indicate that C-BF can prevent gut barrier dysfunction induced by LPS, suggesting that C-BF may be used to develop a prophylactic agent for intestinal injury in endotoxemia.

Study Information

Provider

pubmed

Year

2015

Date

2015-01-29T00:00:00.000Z

DOI

10.1016/j.intimp.2015.01.017

Citations

55

References

34