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LL-37

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

Quick Stats
Studies 2230
Trials 95
Score 3
2006 pubmed 124 citations

Innate immune peptide LL-37 displays distinct expression pattern from beta-defensins in inflamed gingival tissue.

Hosokawa. I I; Hosokawa. Y Y; Komatsuzawa. H H; Goncalves. R B RB; Karimbux. N N; Napimoga. M H MH; Seki. M M; Ouhara. K K; Sugai. M M; Taubman. M A MA; Kawai. T T

Key Findings

  • Neutrophils in inflamed gingival tissue produce LL‑37 but not beta‑defensins
  • Gingival epithelial cells produce LL‑37 and beta‑defensins whether or not the tissue is inflamed
  • LL‑37 levels in gum tissue rise in proportion to pocket depth and are increased by bacterial stimulation

Practical Outcomes

  • Focus on oral hygiene and strategies that may boost LL‑37, such as adequate vitamin D, regular flossing, and possibly using mouthwashes that support innate immunity. Reducing gum inflammation could lower systemic inflammatory load, benefiting overall health and longevity.

Summary

The study shows that the antimicrobial peptide LL‑37 is especially made by immune cells in inflamed gums and its amount grows with the severity of gum disease, while gum lining cells always make it regardless of inflammation. This suggests LL‑37 plays a key role in oral immunity and could be a target for keeping gums healthy, which may affect overall inflammation and health.

Abstract

Anti-microbial peptides produced from mucosal epithelium appear to play pivotal roles in the host innate immune defence system in the oral cavity. In particular, human beta-defensins (hBDs) and the cathelicidin-type anti-microbial peptide, LL-37, were reported to kill periodontal disease-associated bacteria. In contrast to well-studied hBDs, little is known about the expression profiles of LL-37 in gingival tissue. In this study, the anti-microbial peptides expressed in gingival tissue were analysed using immunohistochemistry and enxyme-linked immunosorbent assay (ELISA). Immunohistochemistry revealed that neutrophils expressed only LL-37, but not hBD-2 or hBD-3, and that such expression was prominent in the inflammatory lesions when compared to healthy gingivae which showed very few or no LL-37 expressing neutrophils. Gingival epithelial cells (GEC), however, expressed all three examined anti-microbial peptides, irrespective of the presence or absence of inflammation. Moreover, as determined by ELISA, the concentration of LL-37 in the gingival tissue homogenates determined was correlated positively with the depth of the gingival crevice. Stimulation with periodontal bacteria in vitro induced both hBD-2 and LL-37 expressions by GEC, whereas peripheral blood neutrophils produced only LL-37 production, but not hBD-2, in response to the bacterial stimulation. These findings suggest that LL-37 displays distinct expression patterns from those of hBDs in gingival tissue.

Study Information

Provider

pubmed

Year

2006

Date

2006-11-01T00:00:00.000Z

DOI

10.1111/j.1365-2249.2006.03200.x

Citations

124

References

37