ArticlePloS one2010
IL-16 promotes T. whipplei replication by inhibiting phagosome conversion and modulating macrophage activation.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Article
- Article
- Aberrant adaptive immune response underlies genetic susceptibility to tuberculosis.Frontiers in immunology · 2024Article
- Uptake ofInternational journal of molecular sciences · 2023Article
- Single-cell and spatiotemporal transcriptomic analyses reveal the effects of microorganisms on immunity and metabolism in the mouse liver.Computational and structural biotechnology journal · 2023Article
- Current knowledge of the immune reconstitution inflammatory syndrome in Whipple disease: a review.Frontiers in immunology · 2023Review
- Whipple's disease: a fatal mimic.Autopsy & case reports · 2021Article
- Triggering MSR1 promotes JNK-mediated inflammation in IL-4-activated macrophages.The EMBO journal · 2019Article
- [The rich diversity of Whipple's disease].Zeitschrift fur Rheumatologie · 2019Review
- Bladder Cancer Exhibiting High Immune Infiltration Shows the Lowest Response Rate to Immune Checkpoint Inhibitors.Frontiers in oncology · 2019Article
- Eosinophil Activation by Toll-Like Receptor 4 Ligands Regulates Macrophage Polarization.Frontiers in cell and developmental biology · 2019Article
- Non-neoplastic histiocytic and dendritic cell disorders in lymph nodes.Seminars in diagnostic pathology · 2018Review
- Clinical Manifestations, Treatment, and Diagnosis of Tropheryma whipplei Infections.Clinical microbiology reviews · 2017Review
- Genome-wide non-CpG methylation of the host genome during M. tuberculosis infection.Scientific reports · 2016Article
- -295 T-to-C promoter region IL-16 gene polymorphism is associated with Whipple's disease.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2015Article
- Investigation of microRNAs in mouse macrophage responses to lipopolysaccharide-stimulation by combining gene expression with microRNA-target information.BMC genomics · 2015Article
- Whipple's Disease.Viszeralmedizin · 2014Review
- Article
- Coxiella burnetii lipopolysaccharide blocks p38α-MAPK activation through the disruption of TLR-2 and TLR-4 association.Frontiers in cellular and infection microbiology · 2014Article
- The complexity of Rab5 to Rab7 transition guarantees specificity of pathogen subversion mechanisms.Frontiers in cellular and infection microbiology · 2014Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The replication of Tropheryma whipplei (the agent of Whipple's disease) within human macrophages is associated with the expression of IL-16, a cytokine known for its chemotactic and inflammatory properties. In this study, we asked whether IL-16 acts on T. whipplei replication by interfering with the endocytic pathway. We observed that in macrophages, T. whipplei was located within late phagosomes that were unable to fuse with lysosomes; in monocytes, T. whipplei was eliminated in phagolysosomes. Moreover, adding IL-16 to monocytes induced bacterial replication and inhibited phagolysosome formation. On the other hand, blocking IL-16 activity, either with anti-IL-16 antibodies in human macrophages or by using murine IL-16(-/-) bone marrow-derived macrophages, inhibited T. whipplei replication and rescued phagolysosome biogenesis. Furthermore, we propose that IL-16-mediated interference with the endocytic pathway is likely related to macrophage activation. First, IFNγ induced T. whipplei elimination and phagolysosome formation and inhibited IL-16 production by macrophages. Second, the full transcriptional response of murine macrophages to T. whipplei showed that T. whipplei specifically modulated the expression of 231 probes in IL-16(-/-) macrophages. Gene Ontology analysis revealed that 10 of 13 over-represented terms were linked to immune responses, including proinflammatory transcriptional factors of the NF-κB family. Our results demonstrated a previously unreported function for IL-16 in promoting bacterial replication through inhibited phagolysosome biogenesis and modulated macrophage activation program.
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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.