Menu
Peptide Database
Results
No peptides found
Featured

Use search to browse all 100+ peptides

LL-37

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

Quick Stats
Studies 2230
Trials 95
Score 2
2011 pubmed 63 citations

Effects of bacterial infection on airway antimicrobial peptides and proteins in COPD.

Parameswaran. Ganapathi Iyer GI; Sethi. Sanjay S; Murphy. Timothy F TF

Key Findings

  • LL‑37 levels increase during bacterial exacerbations in COPD
  • Lysozyme levels decrease during colonization and exacerbation
  • SLPI levels drop during exacerbations and colonization by certain bacteria
  • Lactoferrin levels stay about the same

Practical Outcomes

  • The rise in LL‑37 shows it may help clear infections, so biohackers might be interested in ways to support this peptide naturally. However, the research doesn’t provide a specific dosage or supplement strategy, so any attempts to boost LL‑37 remain experimental.

Summary

In people with COPD, when new harmful bacteria show up in the lungs, the natural antimicrobial peptide LL‑37 goes up during flare‑ups, while other defense proteins like lysozyme and SLPI tend to drop. This suggests LL‑37 is part of the body’s immediate response to infection, but the study didn’t test any treatments or supplements.

Abstract

Pathogenic bacteria colonize the airways of 30% to 40% of patients with COPD and cause approximately 50% of exacerbations. New strains of nontypeable Haemophilus influenzae (NTHI) and Moraxella catarrhalis are associated with exacerbations. Antimicrobial protein/peptides (AMPs) play important roles in innate lung defense against pathogens. To our knowledge, the changes in AMP baseline levels in respiratory secretions during bacterial colonization and exacerbation have not been described. The objective of this study was to elucidate the effects of the acquisition of a new strain of pathogenic bacteria on the airway levels of AMPs in patients with COPD. One hundred fifty-three samples from 11 patients were selected from COPD sputum samples collected prospectively over 6 years. Samples were grouped as culture-negative (no pathogenic bacteria), colonization, and exacerbation due to new strains of NTHI and M catarrhalis. Levels of lysozyme, lactoferrin, LL-37, and secretory leukocyte protease inhibitor (SLPI) were measured by enzyme-linked immunosorbent assay and compared among groups by paired analysis. Compared with baseline, sputum lysozyme levels were significantly lower during colonization and exacerbation by NTHI (P = .001 and P = .013, respectively) and M catarrhalis (P = .007 and P = .018, respectively); SLPI levels were lower with exacerbation due to NTHI and M catarrhalis (P = .002 and P = .004, respectively), and during colonization by M catarrhalis (P = 032). Lactoferrin levels did not change significantly; LL-37 levels were higher during exacerbation by NTHI and M catarrhalis (P = .001 and P = .018, respectively). Acquisition of NTHI and M catarrhalis is associated with significant changes in airway levels of AMPs, with larger changes in exacerbation. Airway AMP levels are likely to be important in pathogen clearance and clinical outcomes of infection in COPD.

Study Information

Provider

pubmed

Year

2011

Date

2011-02-24T00:00:00.000Z

DOI

10.1378/chest.10-2760

Citations

63

References

44