# Immunomodulatory Effects of the Antimicrobial Peptide KR-20: Implications for Trichomoniasis

**Authors:** María G. Ramírez-Ledesma, Eva E. Ávila, Nayeli Alva-Murillo

PMC · DOI: 10.3390/molecules31030413 · Molecules · 2026-01-26

## TL;DR

This study explores how the antimicrobial peptide KR-20 affects monocyte immune responses during trichomoniasis, suggesting it could be a new treatment option.

## Contribution

KR-20 is shown to modulate monocyte immune responses during T. vaginalis infection, offering a potential new therapeutic approach.

## Key findings

- KR-20 preserves monocyte metabolic activity and reduces parasite-induced nitric oxide production.
- KR-20 downregulates the expression of IL-8, TNF-α, IL-1β, and COX-2 in infected monocytes.
- KR-20 binds microbial components like LPS and shows potential as an immunomodulatory agent for trichomoniasis.

## Abstract

Trichomoniasis is the most prevalent non-viral sexually transmitted infection worldwide and is caused by Trichomonas vaginalis. The development of resistance against the standard treatment, metronidazole, highlights the need for alternative therapeutic approaches. The role of innate immune cells is crucial for understanding trichomoniasis; however, the contribution of monocytes remains poorly characterized. We previously reported that the antimicrobial peptides LL-37 and its derivative KR-20 are trichomonacidal. In other systems, LL-37 displays immunomodulatory effects. Nevertheless, whether these peptides modulate monocyte responses in the presence of T. vaginalis remains unknown, which was the aim of this study. U937 monocytes were co-incubated with LL-37 or KR-20 (3 h), with or without parasite. Monocyte metabolic activity, nitric oxide production, and relative expression of innate immune genes were assessed. LL-37 decreased monocyte metabolic activity and upregulated TNF-α expression (10 and 5 μM, respectively) in parasite-challenged monocytes. Meanwhile, KR-20 (2.5–10 μM) preserved metabolic activity, bound microbial components (LPS), reduced parasite-induced nitric oxide production, and downregulated the expression of IL-8, TNF-α, IL-1β, and COX-2 in infected monocytes. This work provides initial evidence that KR-20 modulates innate immune response in monocytes during T. vaginalis infection, suggesting its potential—yet to be fully validated—as an immunomodulatory candidate for trichomoniasis.

## Linked entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124], CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576], IL1B (interleukin 1 beta) [NCBI Gene 3553], COX2 (cytochrome c oxidase subunit II) [NCBI Gene 4513]
- **Proteins:** CAMP (cathelicidin antimicrobial peptide)
- **Chemicals:** metronidazole (PubChem CID 4173)
- **Diseases:** trichomoniasis (MONDO:0002154)
- **Species:** Trichomonas vaginalis (taxon 5722)

## Full-text entities

- **Diseases:** T. vaginalis infection (MESH:D007239), Trichomoniasis (MESH:D014245), sexually transmitted infection (MESH:D012749)
- **Chemicals:** metronidazole (MESH:D008795), KR-20 (-), nitric oxide (MESH:D009569), LPS (MESH:D008070)
- **Species:** Trichomonas vaginalis (species) [taxon 5722]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12898638/full.md

## References

113 references — full list in the complete paper: https://tomesphere.com/paper/PMC12898638/full.md

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Source: https://tomesphere.com/paper/PMC12898638