Evidence map›Paper›PMID 28074867›Full record

ArticleScientific reports2017

The role of macrophages in the susceptibility of Fc gamma receptor IIb deficient mice to Cryptococcus neoformans.

Saowapha Surawut, Thunnicha Ondee, Sujittra Taratummarat, Tanapat Palaga, Prapaporn Pisitkun, Ariya Chindamporn, Asada Leelahavanichkul

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Inbred Mouse Models inJournal of fungi (Basel, Switzerland) · 2024
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  4. Journal of fungi (Basel, Switzerland) · 2023
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  9. Prominent Indomethacin-Induced Enteropathy in FcgriibInternational journal of molecular sciences · 2021
    Article
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  15. Article
  16. Article
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  18. Article
  19. Frontiers in microbiology · 2018
    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

7 authors at 2 institutions in 1 country.

Saowapha SurawutMedical Microbiology, Interdisciplinary Program, Graduate School, Chulalongkorn University, Bangkok, Thailand.
Thunnicha OndeeMedical Sciences Program, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Sujittra TaratummaratMedical Microbiology, Interdisciplinary Program, Graduate School, Chulalongkorn University, Bangkok, Thailand.
Tanapat PalagaDepartment of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Prapaporn PisitkunDivision of Allergy, Immunology, and Rheumatology, Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand.
Ariya ChindampornDepartment of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Asada LeelahavanichkulDepartment of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Chulalongkorn University · THRamathibodi Hospital · TH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysfunctional polymorphisms of FcγRIIb, an inhibitory receptor, are associated with Systemic Lupus Erythaematosus (SLE). Cryptococcosis is an invasive fungal infection in SLE, perhaps due to the de novo immune defect. We investigated cryptococcosis in the FcγRIIb-/- mouse-lupus-model. Mortality, after intravenous C. neoformans-induced cryptococcosis, in young (8-week-old) and older (24-week-old) FcγRIIb-/- mice, was higher than in age-matched wild-types. Severe cryptococcosis in the FcγRIIb-/- mice was demonstrated by high fungal burdens in the internal organs with histological cryptococcoma-like lesions and high levels of TNF-α and IL-6, but not IL-10. Interestingly, FcγRIIb-/- macrophages demonstrated more prominent phagocytosis but did not differ in killing activity in vitro and the striking TNF-α, IL-6 and IL-10 levels, compared to wild-type cells. Indeed, in vivo macrophage depletion with liposomal clodronate attenuated the fungal burdens in FcγRIIb-/- mice, but not wild-type mice. When administered to wild-type mice, FcγRIIb-/- macrophages with phagocytosed Cryptococcus resulted in higher fungal burdens than FcγRIIb+/+ macrophages with phagocytosed Cryptococcus. These results support, at least in part, a model whereby, in FcγRIIb-/- mice, enhanced C. neoformans transmigration occurs through infected macrophages. In summary, prominent phagocytosis, with limited effective killing activity, and high pro-inflammatory cytokine production by FcγRIIb-/- macrophages were correlated with more severe cryptococcosis in FcγRIIb-/- mice.

Indexed as

AgingAnimalsBrainCryptococcosisCryptococcus neoformansDisease SusceptibilityFemaleInterleukin-6KidneyLungLupus Erythematosus, SystemicMacrophagesMiceMice, Inbred C57BLMice, KnockoutPhagocytosisFc gamma receptor IIBInterleukin-6Receptors, IgGTumor Necrosis Factor-alpha

Identifiers

PMID28074867
PMCPMC5225418
OpenAlexW2576679261

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.