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Study · In vitro (cells) · 2005

10 results

The human beta-defensins (-1, -2, -3, -4) and cathelicidin LL-37 induce IL-18 secretion through p38 and ERK MAPK activation in primary human keratinocytes.

Niyonsaba F, Ushio H, Nagaoka I, Okumura K, Ogawa H

Journal of immunology (Baltimore, Md. : 1950)1 Aug 2005Cited by 190 (Europe PMC)

PMID16034119 (opens in a new tab)DOI10.4049/jimmunol.175.3.1776 (opens in a new tab)PepBankPUB-16034119
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study10

7 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Activity measurement

    In normal human keratinocytes, LL‑37 activated secretion of IL-18, with peak strength at 3 h.

    In plain wordsIn cells, LL‑37 made human skin cells release more IL-18, an immune signal, with a peak at 3 h.

    Peptide
    LL-37
    Outcome
    IncreaseIL-18 secretion
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Measurements

    Time to peak IL-18 secretion
    3 h
    keratinocytes

    Source sentences

    Summary
    We found that hBD-2, -3, and -4 and LL-37, but not hBD-1, activated normal human keratinocytes to secrete IL-18; this secretion reached peak strength at 3 h
  2. 02LabIn vitro (cells)Mechanism

    In normal human keratinocytes, LL‑37 increased IL-18 mRNA expression.

    In plain wordsIn cells, LL‑37 raised IL-18 gene activity in human skin cells.

    Peptide
    LL-37
    Outcome
    IncreaseIL-18 mRNA expression
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We also revealed that hBD-2, -3, and -4 and LL-37 increased IL-18 mRNA expression
  3. 03LabIn vitro (cells)Mechanism

    In keratinocytes, caspase-1 or caspase family inhibitors could not suppress LL‑37-induced IL-18 secretion.

    In plain wordsIn cells, blocking caspase enzymes did not stop LL‑37 from causing IL-18 release.

    Peptide
    LL-37
    Outcome
    No significant changeCaspase inhibitor effect on IL-18 secretion
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    because IL-18 secretion induced by hBDs and LL-37 could not be suppressed by caspase-1 or caspase family inhibitors
  4. 04LabIn vitro (cells)Mechanism

    In keratinocytes, LL‑37 failed to increase caspase-1 activity.

    In plain wordsIn cells, LL‑37 did not raise the activity of the caspase-1 enzyme.

    Peptide
    LL-37
    Outcome
    No significant changeCaspase-1 activity
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and because these peptides failed to increase caspase-1 activity
  5. 05LabIn vitro (cells)Mechanism

    In keratinocytes, LL‑37 induced phosphorylation of p38.

    In plain wordsIn cells, LL‑37 switched on the p38 signalling protein.

    Peptide
    LL-37
    Outcome
    Increasep38 phosphorylation
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, hBD-2, -3, and -4 and LL-37 could induce the phosphorylation of p38 and ERK1/2, but not JNK.
  6. 06LabIn vitro (cells)Mechanism

    In keratinocytes, LL‑37 induced phosphorylation of ERK1/2.

    In plain wordsIn cells, LL‑37 switched on the ERK1/2 signalling proteins.

    Peptide
    LL-37
    Outcome
    IncreaseERK1/2 phosphorylation
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, hBD-2, -3, and -4 and LL-37 could induce the phosphorylation of p38 and ERK1/2, but not JNK.
  7. 07LabIn vitro (cells)Mechanism

    In keratinocytes, LL‑37 did not induce phosphorylation of JNK.

    In plain wordsIn cells, LL‑37 did not switch on the JNK signalling protein.

    Peptide
    LL-37
    Outcome
    No significant changeJNK phosphorylation
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, hBD-2, -3, and -4 and LL-37 could induce the phosphorylation of p38 and ERK1/2, but not JNK.

Studies that did not test the peptide alone3

In this study, LL-37 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking LL-37.

  1. 08LabNot a test of LL-37 aloneIn vitro (cells)Mechanism

    IL-18 secretion induced by the peptides, which included LL‑37, was more enhanced in keratinocytes differentiated in vitro with high Ca2+-containing medium.

    In plain wordsIn cells, IL-18 release triggered by these peptides, including LL‑37, was stronger in skin cells matured in high-calcium medium.

    Peptide
    LL-37
    Outcome
    IncreaseIL-18 secretion in differentiated keratinocytes
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    and that IL-18 secretion was more enhanced in keratinocytes differentiated in vitro with high Ca2+-containing medium.

    In this study, LL-37 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking LL-37.

  2. 09LabNot a test of LL-37 aloneIn vitro (cells)Mechanism

    In keratinocytes, inhibitors of p38 and ERK1/2 almost completely nullified peptide-induced IL-18 secretion.

    In plain wordsIn cells, blocking the p38 and ERK1/2 pathways almost fully stopped the IL-18 release caused by these peptides.

    Peptide
    LL-37
    Outcome
    Not applicablep38 and ERK1/2 inhibitor effect on IL-18 secretion
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    To determine the molecular mechanism involved, we demonstrated that IL-18 secretion was through p38 and ERK1/2 MAPK pathways, because the inhibitors of p38 and ERK1/2, but not JNK, almost completely nullified IL-18 secretion.

    In this study, LL-37 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking LL-37.

  3. 10LabNot a test of LL-37 aloneIn vitro (cells)Mechanism

    In keratinocytes, a JNK inhibitor did not nullify peptide-induced IL-18 secretion.

    In plain wordsIn cells, blocking the JNK pathway did not stop the IL-18 release caused by these peptides.

    Peptide
    LL-37
    Outcome
    No significant changeJNK inhibitor effect on IL-18 secretion
    Study

    humann: not reported in source

    Primary normal human keratinocytes
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    To determine the molecular mechanism involved, we demonstrated that IL-18 secretion was through p38 and ERK1/2 MAPK pathways, because the inhibitors of p38 and ERK1/2, but not JNK, almost completely nullified IL-18 secretion.

    In this study, LL-37 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking LL-37.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 3Current

    9 Oct 2026, 18:17 UTC

    Study results updated

  2. Version 2

    9 Oct 2026, 03:03 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 02:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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