Human β defensin-3 induces chemokines from monocytes and macrophages: diminished activity in cells from HIV-infected persons.
Petrov. Velizar V; Funderburg. Nicholas N; Weinberg. Aaron A; Sieg. Scott S
Key Findings
- LL‑37 modestly induces chemokines in monocytes, but less effectively than hBD‑3.
- Monocytes from HIV‑positive donors spontaneously produce certain chemokines and respond less to hBD‑3 for others.
- Chemokine receptor levels are mostly normal in HIV‑positive cells, except for a drop in CCR4 on a specific monocyte subset.
Practical Outcomes
- For most biohackers, the findings don’t translate into actionable protocols or dosage advice for LL‑37. The research mainly adds to basic science knowledge about immune signaling and highlights altered responses in HIV infection, which isn’t directly useful for longevity or performance optimization.
Summary
The study looked at how a few immune‑boosting peptides, including LL‑37, affect immune cells. It found that LL‑37 can trigger some signaling molecules, but it’s not as strong as another peptide (hBD‑3). People with HIV showed different immune responses, but the work doesn’t give clear guidance for everyday use.
Abstract
Human β defensin-3 (hBD-3) is an antimicrobial peptide with diverse functionality. We investigated the capacity of hBD-3 and, for comparison, Pam3CSK4 and LL-37 to induce co-stimulatory molecules and chemokine expression in monocytes. These stimuli differentially induced CD80 and CD86 on the surface of monocytes and each stimulant induced a variety of chemokines including monocyte chemoattractant protein 1 (MCP-1), Gro-α, macrophage-derived chemokine (MDC) and macrophage inflammatory protein 1β (MIP1β), while only hBD-3 and Pam3CSK4 significantly induced the angiogenesis factor, vascular endothelial growth factor (VEGF). Human BD-3 induced similar chemokines in monocyte-derived macrophages and additionally induced expression of Regulated upon activation normal T-cell expressed and presumably secreted (RANTES) in these cells. Comparison of monocytes from HIV(+) and HIV(-) donors indicated that monocytes from HIV(+) donors were more likely to spontaneously express certain chemokines (MIP-1α, MIP-1β and MCP-1) and less able to increase expression of other molecules in response to hBD-3 (MDC, Gro-α and VEGF). Chemokine receptor expression (CCR5, CCR2 and CXCR2) was relatively normal in monocytes from HIV(+) donors compared with cells from HIV(-) donors with the exception of diminished expression of the receptor for MDC, CCR4, which was reduced in the patrolling monocyte subset (CD14(+)  CD16(++) ) of HIV(+) donors. These observations implicate chemokine induction by hBD-3 as a potentially important mechanism for orchestrating cell migration into inflamed tissues. Alterations in chemokine production or their receptors in monocytes of HIV-infected persons could influence cell migration and modify the effects of hBD-3 at sites of inflammation.
Study Information
pubmed
2013
2013-12-01T00:00:00.000Z
10.1111/imm.12148
39
30