Evidence map›Paper›PMID 26285576›Full record

ArticleBMC infectious diseases2015

Alpha7 nicotinic acetylcholine receptor is required for blood-brain barrier injury-related CNS disorders caused by Cryptococcus neoformans and HIV-1 associated comorbidity factors.

Bao Zhang, Jing-Yi Yu, Li-Qun Liu, Liang Peng, Feng Chi, Chun-Hua Wu, Ambrose Jong, Shi-Fu Wang, Hong Cao, Sheng-He Huang

Open access · goldAbstract read
In one paragraph

Article in BMC infectious diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. [Indole-3-acetic acid alleviatesNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Bidirectional Associations among Nicotine and Tobacco Smoke, NeuroHIV, and Antiretroviral Therapy.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  13. [Establishment of a gp120 transgenic mouse model withNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Bao ZhangDepartment of Microbiology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, 510515, China. zhang20051005@126.com.
Jing-Yi YuDepartment of Microbiology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, 510515, China. jyyu1001@126.com.
Li-Qun LiuDivision of Pediatric Neurology, Children's Medical Center, The Second Xiangya Hospital of Central South University, Changsha, Hunan, 410011, China. llq91217@163.com.
Liang PengSaban Research Institute of Childrens Hospital Los Angeles, Department of Pediatrics, University of Southern California, 4650 Sunset Blvd., Mailstop #51, Los Angeles, CA, 90027, USA. lapeng@chla.usc.edu.
Feng ChiSaban Research Institute of Childrens Hospital Los Angeles, Department of Pediatrics, University of Southern California, 4650 Sunset Blvd., Mailstop #51, Los Angeles, CA, 90027, USA. chifeng68@gmail.com.
Chun-Hua WuSaban Research Institute of Childrens Hospital Los Angeles, Department of Pediatrics, University of Southern California, 4650 Sunset Blvd., Mailstop #51, Los Angeles, CA, 90027, USA. CWu@chla.usc.edu.
Ambrose JongSaban Research Institute of Childrens Hospital Los Angeles, Department of Pediatrics, University of Southern California, 4650 Sunset Blvd., Mailstop #51, Los Angeles, CA, 90027, USA. ajong@chla.usc.edu.
Shi-Fu WangSaban Research Institute of Childrens Hospital Los Angeles, Department of Pediatrics, University of Southern California, 4650 Sunset Blvd., Mailstop #51, Los Angeles, CA, 90027, USA. shiwang@chla.usc.edu.
Hong CaoDepartment of Microbiology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, 510515, China. gzhcao@smu.edu.cn.
Sheng-He HuangDepartment of Microbiology, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, 510515, China. shhuang@hsc.usc.edu.
University of Southern California · USSouthern Medical University · CNCentral South University · CNQilu Hospital of Shandong University · CN

Funding

Invasion of C. neoformans into brain endothelial cellsR01NS047599 · NINDS · CHILDREN'S HOSPITAL OF LOS ANGELES · PI JONG, AMBROSE Y · 2004 to 2012
$2.5M
Identification of Biomarkers for BBB Injury-Induced by Drugs and HIV-1 ProteinsR03DA034515 · NIDA · CHILDREN'S HOSPITAL OF LOS ANGELES · PI HUANG, SHENG-HE · 2013 to 2014
$162k
NIDA NIH HHS R03-DA03451NIDA NIH HHS R03 DA034515NINDS NIH HHS R01 NS047599NINDS NIH HHS R01-NS047599
6 · The paper itself

Abstract

backgroundCryptococcal meningitis is the most common fungal infection of the central nervous system (CNS) in HIV/AIDS. HIV-1 virotoxins (e.g., gp41) are able to induce disorders of the blood-brain barrier (BBB), which mainly consists of BMEC. Our recent study suggests that α7 nAChR is an essential regulator of inflammation, which contributes to regulation of NF-κB signaling, neuroinflammation and BBB disorders caused by microbial (e.g., HIV-1 gp120) and non-microbial [e.g., methamphetamine (METH)] factors. However, the underlying mechanisms for multiple comorbidities are unclear.

methodsIn this report, an aggravating role of α7 nAChR in host defense against CNS disorders caused by these comorbidities was demonstrated by chemical [inhibitor: methyllycaconitine (MLA)] and genetic (α7(-/-) mice) blockages of α7 nAChR.

resultsAs shown in our in vivo studies, BBB injury was significantly reduced in α7(-/-) mice infected with C. neoformans. Stimulation by the gp41 ectodomain peptide (gp41-I90) and METH was abolished in the α7(-/-) animals. C. neoformans and gp41-I90 could activate NF-κB. Gp41-I90- and METH-induced monocyte transmigration and senescence were significantly inhibited by MLA and CAPE (caffeic acid phenethyl ester, an NF-κB inhibitor).

conclusionsCollectively, our data suggest that α7 nAChR plays a detrimental role in the host defense against C. neoformans- and HIV-1 associated comorbidity factors-induced BBB injury and CNS disorders.

Indexed as

Cryptococcus neoformansAconitinealpha7 Nicotinic Acetylcholine ReceptorAnimalsBlood-Brain BarrierCentral Nervous System StimulantsCoinfectionHIV-1HIV Envelope Protein gp41HIV InfectionsInflammationMeningitis, CryptococcalMethamphetamineMiceMice, KnockoutNF-kappa BAconitinealpha7 Nicotinic Acetylcholine ReceptorCentral Nervous System StimulantsChrna7 protein, mousegp41 protein, Human immunodeficiency virus 1HIV Envelope Protein gp41MethamphetaminemethyllycaconitineNF-kappa BNicotinic Antagonists

Identifiers

PMID26285576
PMCPMC4543465
OpenAlexW2142131754

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.