ArticlePLoS pathogens2017
The macrophage cytoskeleton acts as a contact sensor upon interaction with Entamoeba histolytica to trigger IL-1β secretion.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- Extracellular vesicles in intestinal protozoa: hidden mediators of host-parasite communication.Gut pathogens · 2025Review
- Molecular regulation of NLRP3 inflammasome activation during parasitic infection.Bioscience reports · 2024Review
- Extracellular Vesicles Derived FromJournal of parasitology research · 2024Article
- The colonic pathogen Entamoeba histolytica activates caspase-4/1 that cleaves the pore-forming protein gasdermin D to regulate IL-1β secretion.PLoS pathogens · 2022Article
- Microtubule affinity regulating kinase 4 promoted activation of the NLRP3 inflammasome-mediated pyroptosis in periodontitis.Journal of oral microbiology · 2022Article
- A Src-H3 acetylation signaling axis integrates macrophage mechanosensation with inflammatory response.Biomaterials · 2021Article
- Article
- Entamoeba histolytica exploits the autophagy pathway in macrophages to trigger inflammation in disease pathogenesis.Mucosal immunology · 2021Article
- Entamoeba histolytica activation of caspase-1 degrades cullin that attenuates NF-κB dependent signaling from macrophages.PLoS pathogens · 2021Article
- Host Protective Mechanisms to Intestinal Amebiasis.Trends in parasitology · 2021Review
- The NF-κB Pathway: Modulation byFrontiers in cellular and infection microbiology · 2021Review
- ArfX2 GTPase Regulates Trafficking From the Trans-Golgi to Lysosomes and Is Necessary for Liver Abscess Formation in the Protozoan ParasiteFrontiers in cellular and infection microbiology · 2021Article
- A Novel TLR4-Binding Domain of Peroxiredoxin FromFrontiers in immunology · 2021Article
- Entamoeba histolytica stimulates the alarmin molecule HMGB1 from macrophages to amplify innate host defenses.Mucosal immunology · 2020Article
- Entamoeba histolytica Interaction with Enteropathogenic Escherichia coli Increases Parasite Virulence and Inflammation in Amebiasis.Infection and immunity · 2019Article
- Downregulation of calponin 2 contributes to the quiescence of lung macrophages.American journal of physiology. Cell physiology · 2019Article
- Entamoeba histolytica-induced IL-1β secretion is dependent on caspase-4 and gasdermin D.Mucosal immunology · 2019Article
- Peroxisome proliferator-activated receptor γ (PPARγ) induces the gene expression of integrin αThe Journal of biological chemistry · 2018Article
- Cysteine proteases in protozoan parasites.PLoS neglected tropical diseases · 2018Review
- Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Entamoeba histolytica (Eh) is the causative agent of amebiasis, one of the major causes of dysentery-related morbidity worldwide. Recent studies have underlined the importance of the intercellular junction between Eh and host cells as a determinant in the pathogenesis of amebiasis. Despite the fact that direct contact and ligation between Eh surface Gal-lectin and EhCP-A5 with macrophage α5β1 integrin are absolute requirements for NLRP3 inflammasome activation and IL-1β release, many other undefined molecular events and downstream signaling occur at the interface of Eh and macrophage. In this study, we investigated the molecular events at the intercellular junction that lead to recognition of Eh through modulation of the macrophage cytoskeleton. Upon Eh contact with macrophages key cytoskeletal-associated proteins were rapidly post-translationally modified only with live Eh but not with soluble Eh proteins or fragments. Eh ligation with macrophages rapidly activated caspase-6 dependent cleavage of the cytoskeletal proteins talin, Pyk2 and paxillin and caused robust release of the pro-inflammatory cytokine, IL-1β. Macrophage cytoskeletal cleavages were dependent on Eh cysteine proteinases EhCP-A1 and EhCP-A4 but not EhCP-A5 based on pharmacological blockade of Eh enzyme inhibitors and EhCP-A5 deficient parasites. These results unravel a model where the intercellular junction between macrophages and Eh form an area of highly interacting proteins that implicate the macrophage cytoskeleton as a sensor for Eh contact that leads downstream to subsequent inflammatory immune responses.
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