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LL-37

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

Quick Stats
Studies 2230
Trials 95
Score 2
2017 pubmed 3 citations

Endotoxin Exposure Increases LL-37 - but Not Calprotectin - in Healthy Human Airways.

Smith. Margaretha E ME; Stockfelt. Marit M; Tengvall. Sara S; Bergman. Peter P; Lindén. Anders A; Qvarfordt. Ingemar I

Key Findings

  • Both LL‑37 and calprotectin are normally present in airway fluid.
  • Endotoxin exposure raises neutrophil counts and both the precursor and active forms of LL‑37 after 12 and 24 hours.
  • Calprotectin levels remain unchanged after endotoxin exposure.
  • LL‑37 levels correlate positively with neutrophil numbers, indicating a linked immune response.

Practical Outcomes

  • The study suggests that LL‑37 can be induced locally in the lungs by an innate immune trigger, but using endotoxin is not a safe or practical way to boost it. For biohackers, the finding confirms that LL‑37 is responsive to immune activation, but it offers no actionable protocol for safely increasing LL‑37 levels in humans.

Summary

In healthy people, breathing in a small amount of bacterial toxin (endotoxin) makes the airway release more of the antimicrobial peptide LL‑37, but it doesn't change levels of another peptide, calprotectin. This shows LL‑37 can be quickly turned on by the body's innate immune response in the lungs.

Abstract

The antimicrobial peptides (AMPs) LL-37 and calprotectin are important players in the innate immunity of human airways. In patients with diseases characterized by bacterial colonization, the airway concentrations of these AMPs are increased. Less is known about their presence and release patterns in healthy humans. Our aim was to determine whether LL-37 and calprotectin are released after the activation of the innate immune response in the peripheral airways. Healthy volunteers underwent exposure to endotoxin and vehicle in contralateral segment bronchi. After 12 or 24 h, samples of bronchoalveolar lavage fluid (BALf) were collected bilaterally from exposed segments. Cell and AMP concentrations were assessed, as were the pro-form and active form of LL-37. Both LL-37 and calprotectin were detected in cell-free BALf from both endotoxin- and vehicle-exposed segments. The concentrations of precursor and active LL-37 and neutrophils were significantly higher in endotoxin-exposed segments after 12 and 24 h, and the concentrations of LL-37 and neutrophils correlated positively. The concentrations of calprotectin were not markedly affected by exposure to endotoxin. Local endotoxin exposure elicits the release and activation of LL-37 but not calprotectin in healthy human peripheral airways, suggesting an inducible involvement of LL-37 in the local innate immune response.

Study Information

Provider

pubmed

Year

2017

Date

2017-06-13T00:00:00.000Z

DOI

10.1159/000475525

Citations

3

References

26