ArticleJournal of biomedical science2016
CD44-mediated monocyte transmigration across Cryptococcus neoformans-infected brain microvascular endothelial cells is enhanced by HIV-1 gp41-I90 ectodomain.
Article in Journal of biomedical science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 24 citations in OpenAlex.
- Altered splenic T-cell subpopulation dynamics in a murine model of bovine digital dermatitis-associatedFrontiers in immunology · 2026Article
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- Clinical characteristics and prognostic factors of pulmonary and extrapulmonary cryptococcosis.BMC infectious diseases · 2024Article
- BIOMOLECULAR ACTIVITY OF CRYPTOCOCCUS DURING CRYPTOCOCCOSIS: A REVIEW OF MOLECULAR INTERACTIONS OF CRYPTOCOCCUS WITH HUMAN IMMUNE SYSTEM AND BLOOD-BRAIN-BARRIER.African journal of infectious diseases · 2024Article
- Potential mechanism of TMEM2/CD44 in endoplasmic reticulum stress‑induced neuronal apoptosis in a rat model of traumatic brain injury.International journal of molecular medicine · 2023Article
- Universal method for the isolation of microvessels from frozen brain tissue: A proof-of-concept multiomic investigation of the neurovasculature.Brain, behavior, & immunity - health · 2023Article
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- Host cell membrane microdomains and fungal infection.Cellular microbiology · 2021Review
- In vitro infection models to study fungal-host interactions.FEMS microbiology reviews · 2021Review
- Microglia: The Real Foe in HIV-1-Associated Neurocognitive Disorders?Biomedicines · 2021Review
- Endogenous α7 nAChR Agonist SLURP1 FacilitatesFrontiers in immunology · 2021Article
- COVID-19 severity correlates with airway epithelium-immune cell interactions identified by single-cell analysis.Nature biotechnology · 2020Article
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- New Challenges of HIV-1 Infection: How HIV-1 Attacks and Resides in the Central Nervous System.Cells · 2019Review
- Clinical characteristics and cerebro-spinal fluid cytokine changes in patients with acquired immunodeficiency syndrome and central nervous system infection.Experimental and therapeutic medicine · 2019Article
- Human Immunodeficiency Virus in the Brain-Culprit or Facilitator?Infectious diseases · 2018Review
- Host response to pulmonary fungal infections: A highlight on cell-driven immunity toCurrent pharmacology reports · 2017Article
- [Lactobacillus rhamnosus GG conditioned medium prevents E. coli meningitis by inhibiting nuclear factor-κB pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
- Modeling HIV-1 Induced Neuroinflammation in Mice: Role of Platelets in Mediating Blood-Brain Barrier Dysfunction.PloS one · 2016Article
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCryptococcus neoformans (Cn) is an important opportunistic pathogen in the immunocompromised people, including AIDS patients, which leads to fatal cryptococcal meningitis with high mortality rate. Previous researches have shown that HIV-1 gp41-I90 ectodomain can enhance Cn adhesion to and invasion of brain microvascular endothelial cell (BMEC), which constitutes the blood brain barrier (BBB). However, little is known about the role of HIV-1 gp41-I90 in the monocyte transmigration across Cn-infected BBB. In the present study, we provide evidence that HIV-1 gp41-I90 and Cn synergistically enhance monocytes transmigration across the BBB in vitro and in vivo. The underlying mechanisms for this phenomenon require further study.
methodsIn this study, the enhancing role of HIV-1 gp41-I90 in monocyte transmigration across Cn-infected BBB was demonstrated by performed transmigration assays in vitro and in vivo.
resultsOur results showed that the transmigration rate of monocytes are positively associated with Cn and/or HIV-1 gp41-I90, the co-exposure (HIV-1 gp41-I90 + Cn) group showed a higher THP-1 transmigration rate (P < 0.01). Using CD44 knock-down HBMEC or CD44 inhibitor Bikunin in the assay, the facilitation of transmigration rates of monocyte enhanced by HIV-1 gp41-I90 was significantly suppressed. Western blotting analysis and biotin/avidin enzyme-linked immunosorbent assays (BA-ELISAs) showed that Cn and HIV-1 gp41-I90 could increase the expression of CD44 and ICAM-1 on the HBMEC. Moreover, Cn and/or HIV-1 gp41-I90 could also induce CD44 redistribution to the membrane lipid rafts. By establishing the mouse cryptococcal meningitis model, we found that HIV-1 gp41-I90 and Cn could synergistically enhance the monocytes transmigration, increase the BBB permeability and injury in vivo.
conclusionsCollectively, our findings suggested that HIV-1 gp41-I90 ectodomain can enhance the transmigration of THP-1 through Cn-infected BBB, which may be mediated by CD44. This novel study enlightens the future prospects to elaborate the inflammatory responses induced by HIV-1 gp41-I90 ectodomain and to effectively eliminate the opportunistic infections in AIDS patients.
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