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LL-37

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

Quick Stats
Studies 2230
Trials 95
Score 1
2015 pubmed 44 citations

Recombinant erythroid differentiation regulator 1 inhibits both inflammation and angiogenesis in a mouse model of rosacea.

Kim. Miri M; Kim. Kyung-Eun KE; Jung. Haw Young HY; Jo. Hyunmu H; Jeong. Seo-Won SW; Lee. Jahyung J; Kim. Chang Han CH; Kim. Heejong H; Cho. Daeho D; Park. Hyun Jeong HJ

Key Findings

  • Erdr1 levels are reduced and IL‑18 levels are increased in rosacea patients
  • Injecting LL‑37 into mice creates rosacea‑like skin symptoms
  • Recombinant Erdr1 treatment in mice lessens redness, immune cell infiltration, and VEGF‑driven angiogenesis

Practical Outcomes

  • The findings point to Erdr1 as a possible future skin‑health therapy, but there’s no ready‑to‑use supplement or dosage for self‑experimentation. For now, biohackers should focus on proven anti‑inflammatory and skin‑care strategies rather than trying to use recombinant Erdr1.

Summary

A study found that a protein called Erdr1 is lower in people with rosacea, while the inflammatory molecule IL‑18 is higher. In mice, giving LL‑37 caused rosacea‑like skin redness and blood vessel growth, but treating them with lab‑made Erdr1 reduced the redness, immune cell infiltration, and new blood vessels. This suggests Erdr1 could help calm skin inflammation and blood‑vessel changes in rosacea, but it’s still early‑stage animal work.

Abstract

The erythroid differentiation regulator 1 (Erdr1), which is a novel and highly conserved factor, was recently reported to be negatively regulated by IL-18 and to play a crucial role as an antimetastatic factor. IL-18 is a proinflammatory cytokine that functions as an angiogenic mediator in inflammation. Rosacea is a chronic inflammatory skin disorder that is characterized by abnormal inflammation and vascular hyperactivity of the facial skin. To determine whether Erdr1 contributes to the regulation of the chronic inflammatory process in the development of rosacea, an immunohistochemical analysis was performed in healthy donors and patients with rosacea. In this study, we showed that Erdr1 was downregulated, whereas IL-18 was upregulated, in patients with rosacea, which led us to question the role of Erdr1 in this disorder. Moreover, a rosacea-like BALB/c mouse model was used to determine the role of Erdr1 in rosacea in vivo. LL-37 injection induced typical rosacea features, including erythema, telangiectasia and inflammation. Treatment with recombinant Erdr1 (rErdr1) resulted in a significant reduction of erythema, inflammatory cell infiltration (including CD4(+) and CD8(+) T cells), and microvessel density with vascular endothelial growth factor (VEGF). Taken together, our findings suggest that rErdr1 may be involved in attenuating the inflammation and angiogenesis associated with the pathogenesis of rosacea. Thus, these results provide new insight into the mechanism involved in this condition and indicate that rErdr1 could be a potential target for therapeutic intervention of rosacea.

Study Information

Provider

pubmed

Year

2015

Date

2015-07-14T00:00:00.000Z

DOI

10.1111/exd.12745

Citations

44

References

49