ArticleInflammation2011
Cathelicidin peptide LL-37 modulates TREM-1 expression and inflammatory responses to microbial compounds.
Article in Inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- The role of triggering receptor expressed on myeloid cells-1 (TREM-1) in central nervous system diseases.Molecular brain · 2022Review
- Antimicrobial peptide 17BIPHE2 inhibits the proliferation of lung cancer cellsOncology letters · 2021Article
- Novel ligands and modulators of triggering receptor expressed on myeloid cells receptor family: 2015-2020 updates.Expert opinion on therapeutic patents · 2021Review
- Cathelicidins Modulate TLR-Activation and Inflammation.Frontiers in immunology · 2020Review
- Therapeutic Effect of Modulating TREM-1 via Anti-inflammation and Autophagy in Parkinson's Disease.Frontiers in neuroscience · 2019Article
- Host Defense Peptide LL-37-Mediated Chemoattractant Properties, but Not Anti-Inflammatory Cytokine IL-1RA Production, Is Selectively Controlled by Cdc42 Rho GTPaseFrontiers in immunology · 2018Article
- GPR84 and TREM-1 Signaling Contribute to the Pathogenesis of Reflux Esophagitis.Molecular medicine (Cambridge, Mass.) · 2016Article
- In Vivo Role of TLR2 and MyD88 Signaling in Eliciting Innate Immune Responses in Staphylococcal Endophthalmitis.Investigative ophthalmology & visual science · 2015Article
- Antimicrobial peptide LL-37 along with peptidoglycan drive monocyte polarization toward CD14(high)CD16(+) subset and may play a crucial role in the pathogenesis of psoriasis guttata.American journal of translational research · 2015Article
- Immune modulation by multifaceted cationic host defense (antimicrobial) peptides.Nature chemical biology · 2013Review
- TREM-1 as a potential therapeutic target in psoriasis.The Journal of investigative dermatology · 2013Article
- On the role of NMR spectroscopy for characterization of antimicrobial peptides.Methods in molecular biology (Clifton, N.J.) · 2013Review
- Induction of triggering receptor expressed on myeloid cells (TREM-1) in airway epithelial cells by 1,25(OH)₂ vitamin D₃.Innate immunity · 2012Article
- Inflammatory marker sTREM-1 reflects the clinical stage and respiratory tract obstruction in allergic asthma bronchiale patients and correlates with number of neutrophils.Mediators of inflammation · 2012Article
- Article
- Vitamin D-mediated induction of innate immunity in gingival epithelial cells.Infection and immunity · 2011Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Inflammatory diseases remain an important cause of morbidity and mortality. Cathelicidins are immunomodulatory and antimicrobial peptides with potent anti-endotoxic properties. Although the effects of the human cathelicidin LL-37 on cellular responses to Toll-like receptor (TLR) ligands have been investigated, its effects on responses to other pro-inflammatory stimuli have not been well studied. Triggering receptor expressed on myeloid cells (TREM-1) acts to amplify inflammatory responses and plays important roles in the pathogenesis of endotoxemia. In this work, the effects of LL-37 on responses to TREM-1 stimulation, alone and in the presence of a range of microbial compounds, were analyzed. It was shown that in peripheral blood mononuclear cells LL-37 strongly suppressed synergistic responses to TREM-1 and TLR4 stimulation, partly through the inhibition of TREM-1 expression on monocytes; similar effects were observed using the TLR2 ligand lipoteichoic acid. In contrast, LL-37 stimulated TREM-1 upregulation by peptidoglycan (PGN, TLR2 ligand that is also recognized via nucleotide-binding oligomerization domain containing 2 after fragmentation and intracellular uptake), as well as the responses to combined TREM-1 and PGN stimulation, possibly via the p38 mitogen-activated protein kinase pathway. LL-37 did not affect TREM-1-induced neutrophil degranulation or the production of reactive oxygen species and interleukin-8 by neutrophils. These findings provide further insight into the roles of LL-37 during inflammation and may have implications for its in vivo immunomodulatory properties and for the design of synthetic cathelicidin derivatives as anti-inflammatory and anti-endotoxic molecules.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.