ArticlePloS one2018
HIV induces production of IL-18 from intestinal epithelial cells that increases intestinal permeability and microbial translocation.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Intestinal Epithelial MHC-II at the Interface of Microbiota, Immunity, and Inflammation.International journal of molecular sciences · 2026Review
- Virus-Induced Intestinal Barrier Injury: Mechanisms and Therapeutic Perspectives.Veterinary sciences · 2026Review
- Nanomaterial-Based Strategies Targeting IL-1 Signalling in Inflammatory Bowel Disease: Therapeutic Applications and Mechanistic Insights.Journal of inflammation research · 2026Review
- Macrophage pyroptosis in inflammatory bowel disease: mechanistic insights, pathological roles and treatment strategies.Frontiers in immunology · 2026Review
- Article
- Unique Profile of Proinflammatory Cytokines in Plasma of Drug-Naïve Individuals with Advanced HIV/TB Co-Infection.Viruses · 2023Article
- Analysis of the interferon-γ-induced secretome of intestinal endothelial cells: putative impact on epithelial barrier dysfunction in IBD.Frontiers in cell and developmental biology · 2023Article
- Differential Response to the Course of Cryptosporidium parvum Infection and Its Impact on Epithelial Integrity in Differentiated versus Undifferentiated Human Intestinal Enteroids.Infection and immunity · 2022Article
- Alterations in circulating markers in HIV/AIDS patients with poor immune reconstitution: Novel insights from microbial translocation and innate immunity.Frontiers in immunology · 2022Review
- Cytomegalovirus as an Uninvited Guest in the Response to Vaccines in People Living with HIV.Viruses · 2021Review
- Hyperglycemia minimally alters primary self-renewing human colonic epithelial cells while TNFα-promotes severe intestinal epithelial dysfunction.Integrative biology : quantitative biosciences from nano to macro · 2021Article
- Therapeutic implications of inflammasome in inflammatory bowel disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Review
- Tight Junctions as a Key for Pathogens Invasion in Intestinal Epithelial Cells.International journal of molecular sciences · 2021Review
- Regulation of Intestinal Epithelial Barrier and Immune Function by Activated T Cells.Cellular and molecular gastroenterology and hepatology · 2021Article
- Inflammatory Mechanisms and Cascades Contributing to Neurocognitive Impairment in HIV/AIDS.Current topics in behavioral neurosciences · 2021Article
- A review of potential microbiome-gut-brain axis mediated neurocognitive conditions in persons living with HIV.Brain, behavior, & immunity - health · 2020Review
- Effect of Opioid Use on Immune Activation and HIV Persistence on ART.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020Review
- Association of intestinal and systemic inflammatory biomarkers with immune reconstitution in HIV+ patients on ART.Journal of inflammation (London, England) · 2020Article
- Circulating LPS and (1→3)-β-D-Glucan: A Folie à Deux Contributing to HIV-Associated Immune Activation.Frontiers in immunology · 2019Review
- IL-33 and IL-18 in Inflammatory Bowel Disease Etiology and Microbial Interactions.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-18 (IL-18) is a pleiotropic cytokine of the IL-1 family with multiple context dependent functions. We and others have shown that HIV infection is accompanied by increased circulating levels of IL-18 along with decreased levels of its antagonist, Interleukin-18 Binding Protein (IL-18BP). The infection is also accompanied by intestinal inflammation and decreased intestinal integrity as measured by intestinal permeability, regeneration and repair. However, little is known concerning the relation between high level of IL-18 associated with the viral infection and intestinal permeability. Here we demonstrate that HIV treatment increases production of IL-18 and decreases that of IL-18BP production in human intestinal epithelial cell (IEC) lines. IL-18 causes apoptosis of the IEC by activating caspase-1 and caspase-3. It induces epithelial barrier hyperpermeability by decreasing and disrupting both tight and adherens junction proteins, occludin, claudin 2 and beta-catenin. Disorganization of F-actin was also observed in the IEC that were exposed to the cytokine. Moreover IL-18 decreases transepithelial electrical resistance (TEER) in Caco-2 and increases permeability in HT29 monolayers. The cells' treatment with IL-18 causes an increase in the expression of phosphorylated myosin II regulatory light-chain (p-MLC) and myosin light-chain kinase (MLCK), and a decrease in phosphorylated Signal Transducer and Activator of Transcription (p-STAT)-5. This increase in p-MLC is suppressed by a Rho-kinase (ROCK)-specific inhibitor. Interestingly, the levels of the cytokine correlate with those of LPS in the circulation in three different categories of HIV infected patients (HAART-naïve and HAART-treated HIV-infected individuals, and Elite controls) as well as in healthy controls. Collectively, these results suggest that the HIV-induced IL-18 plays a role in increased intestinal permeability and microbial translocation observed in HIV-infected individuals.
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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.