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LL-37

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

Quick Stats
Studies 2230
Trials 95
Score 2
2004 pubmed

The expression of human antimicrobial peptide LL-37 in the human nasal mucosa.

Chen. Po-Hsu PH; Fang. Sheen-Yie SY

Key Findings

  • LL‑37 mRNA is present in normal human nasal tissue
  • LL‑37 mRNA levels are significantly higher in nasal polyps from sinusitis patients
  • LL‑37 peptide is found in surface epithelial cells and submucosal glands of the nasal mucosa

Practical Outcomes

  • Nasal tissue contributes to innate immune defense via LL‑37, and inflammation boosts its production. For biohackers, this suggests that supporting nasal health (e.g., maintaining clear airways, avoiding irritants) could help maintain natural antimicrobial defenses, though the study does not provide specific dosing or treatment protocols.

Summary

The study shows that the antimicrobial peptide LL‑37 is naturally made in the lining of the nose and that its production goes up when the nose is inflamed, like in people with chronic sinus problems.

Abstract

LL-37, an antimicrobial peptide, has been discovered to be produced by a number of epithelial cells. It is identified as a key element in the innate host defense mechanism. Because little is known about the expression of LL-37 in human sinonasal tract, we conducted this study to investigate the expression of LL-37 in human nasal mucosa. We investigated the expression of LL-37 gene by the reverse transcription polymerase chain reaction (RT-PCR) and localization of LL-37 peptide by immunohistochemistry in the inferior turbinate mucosa of 7 normal subjects and the nasal polyps of 12 patients with chronic paranasal sinusitis. The transcripts of the LL-37 gene were detected in all human nasal tissues analyzed by RT-PCR. There is a significant increase of LL-37 mRNA expression in nasal polyps as compared with the normal nasal mucosa. Using immunohistochemistry, LL-37 peptide was localized in surface epithelial cells and submucosal glands. Our findings suggest that LL-37 is expressed by nasal mucosa and is upregulated during inflammation.

Study Information

Provider

pubmed

Year

2004