ArticleInnate immunity2010
Phospholipase C, p38/MAPK, and NF-kappaB-mediated induction of MIP-3alpha/CCL20 by Porphyromonas gingivalis.
Article in Innate immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Possible immunomodulatory role of Filifactor alocis through beta-defensin 2 in gingival keratinocytes.Clinical oral investigations · 2024Article
- Co-Culture ofInternational journal of molecular sciences · 2024Article
- Oral Microbiota Variation: A Risk Factor for Development and Poor Prognosis of Esophageal Cancer.Digestive diseases and sciences · 2022Review
- Cryptosporidial Infection Suppresses Intestinal Epithelial Cell MAPK Signaling Impairing Host Anti-Parasitic Defense.Microorganisms · 2021Article
- Interferon Regulatory Factor 6 Promotes Keratinocyte Differentiation in Response to Porphyromonas gingivalis.Infection and immunity · 2017Article
- Induction of the inflammatory regulator A20 by gibberellic acid in airway epithelial cells.British journal of pharmacology · 2016Article
- Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells.PloS one · 2016Article
- Genetic variants in PLCB4/PLCB1 as susceptibility loci for coronary artery aneurysm formation in Kawasaki disease in Han Chinese in Taiwan.Scientific reports · 2015Article
- Effect of growth factors on antimicrobial peptides and pro-inflammatory mediators during wound healing.Clinical oral investigations · 2015Article
- Suppression of inflammatory gene expression in T cells by Porphyromonas gingivalis is mediated by targeting MAPK signaling.Cellular & molecular immunology · 2013Article
- Article
- Interplay of protease-activated receptors and NOD pattern recognition receptors in epithelial innate immune responses to bacteria.Immunology letters · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Macrophage inflammatory protein-3alpha/C-C chemokine ligand 20 (MIP-3alpha/CCL20) is an antimicrobial peptide that plays an important role in innate immunity. In addition to direct microbicidal effects, MIP-3alpha/CCL20 also exhibits cytokine-like functions that are critical during dendritic cell activation. The aim of the present study was to investigate further which signaling pathways are involved in the MIP-3alpha/CCL20 mRNA expression in response to whole-cell Porphyromonas gingivalis. Primary gingival epithelial cells (GECs) and the immortalized oral keratinocyte cell-line OKF6/TERT-2 were stimulated with whole-cell P. gingivalis. Prior to stimulation, GECs and OKF6/TERT-2 cells were pretreated with specific inhibitors for nuclear-factor-kappaB (NF-kappaB), mitogen-activated protein kinase (MAPK), phospholipase C (PLC), and phosphatidylinositol-3-kinase (PI3K). In GECs and OKF6/TERT-2 cells, activation of NF-kappaB was examined after exposure to P. gingivalis. The gene expression of MIP-3alpha/CCL20 was significantly induced in response to P. gingivalis (P <or= 0.05) compared to unstimulated control cells. This induction was specifically blocked when cells were pre-incubated with inhibitors for NF-kappaB, MAPK, and PLC (P <or= 0.05), but not for PI3K. These results demonstrate that P. gingivalis induces the MIP-3alpha/CCL20 mRNA in a NF-kappaB-, PLC-, and MAPK-dependent manner.
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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.