Marked reduction of LL-37/hCAP-18, an antimicrobial peptide, in patients with acute myeloid leukemia.
An. Li-Li LL; Ma. Xiao-Tong XT; Yang. Ying-Hua YH; Lin. Yong-Min YM; Song. Yu-Hua YH; Wu. Ke-Fu KF
Key Findings
- AML patients show a marked reduction of LL‑37 protein in neutrophils
- LL‑37 mRNA levels stay the same, indicating the loss is post‑transcriptional
- Stimulating cells with LPS, Staph. aureus, or retinoic acid does not restore LL‑37 levels
Practical Outcomes
- For most biohackers this study isn’t directly actionable, as it focuses on a specific cancer patient group. It does hint that boosting LL‑37 could be a strategy to improve infection resistance, but no proven supplements or protocols are provided.
Summary
People with acute myeloid leukemia have far less of the natural antibiotic peptide LL‑37 in their blood cells, which may help explain why they get infections easily. The drop isn’t because the gene is turned off, and typical lab tricks like adding bacterial components or forcing cells to mature don’t bring the peptide back.
Abstract
We detected LL-37/hCAP-18 expression in the peripheral blood smears of 50 healthy donors and 143 patients with various hematological diseases. Compared with that in the healthy donors, expression of the protein in the neutrophils was significantly lower in patients with acute myeloid leukemia (AML), especially those with infection, but no significant difference was detected in messenger RNA level. We did not detect increased LL-37/hCAP-18 protein expression in U937 cells treated with lipopolysaccharide or Staphylococcus aureus Cowan strain. Furthermore, LL-37/hCAP-18 protein production was not restored in differentiated myeloid cell lines NB4 or HL-60 induced by all-trans retinoic acid. LL-37/hCAP-18 has been shown to play a role in host defense, and its deficiency in AML may be one of the explanations for susceptibility to infection among these patients.
Study Information
pubmed
2005
10.1532/ijh97.a10407