Evidence map›Paper›PMID 35177337›Full record

ArticleCytotherapy2022

Mechanism for the attenuation of neutrophil and complement hyperactivity by MSC exosomes.

Jia Tong Loh, Bin Zhang, Joey Kay Hui Teo, Ruenn Chai Lai, Andre Boon Hwa Choo, Kong-Peng Lam, Sai Kiang Lim

Open access · bronzeAbstract read
In one paragraph

Article in Cytotherapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

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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 1 institution in 1 country.

Jia Tong LohSingapore Immunology Network, Agency for Science, Technology and Research, Republic of Singapore.
Bin ZhangInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, Republic of Singapore.
Joey Kay Hui TeoSingapore Immunology Network, Agency for Science, Technology and Research, Republic of Singapore.
Ruenn Chai LaiInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, Republic of Singapore.
Andre Boon Hwa ChooBioprocessing Technology Institute, Agency for Science, Technology and Research, Republic of Singapore.
Kong-Peng LamSingapore Immunology Network, Agency for Science, Technology and Research, Republic of Singapore; Department of Microbiology and Immunology, Yong Loo Lin School of Medicine, National University of Singapore, Republic of Singapore; School of Biological Sciences, College of Science, Nanyang Technological University, Republic of Singapore. Electronic address: lam_kong_peng@immunol.a-star.edu.sg.
Sai Kiang LimInstitute of Molecular and Cell Biology, Agency for Science, Technology and Research, Republic of Singapore; Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Republic of Singapore. Electronic address: lim_sai_kiang@imcb.a-star.edu.sg.
Agency for Science, Technology and Research · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complements and neutrophils are two key players of the innate immune system that are widely implicated as drivers of severe COVID-19 pathogenesis, as evident by the direct correlation of respiratory failure and mortality with elevated levels of terminal complement complex C5b-9 and neutrophils. In this study, we identified a feed-forward loop between complements and neutrophils that could amplify and perpetuate the cytokine storm seen in severe SARS-CoV-2-infected patients. We observed for the first time that the terminal complement activation complex C5b-9 directly triggered neutrophil extracellular trap (NET) release and interleukin (IL)-17 production by neutrophils. This is also the first report that the production of NETs and IL-17 induced by C5b-9 assembly on neutrophils could be abrogated by mesenchymal stem cell (MSC) exosomes. Neutralizing anti-CD59 antibodies abolished this abrogation. Based on our findings, we hypothesize that MSC exosomes could alleviate the immune dysregulation in acute respiratory failure, such as that observed in severe COVID-19 patients, by inhibiting complement activation through exosomal CD59, thereby disrupting the feed-forward loop between complements and neutrophils to inhibit the amplification and perpetuation of inflammation during SARS-CoV-2 infection.

Indexed as

COVID-19ExosomesMesenchymal Stem CellsComplement Membrane Attack ComplexHumansNeutrophilsSARS-CoV-2Complement Membrane Attack ComplexcomplementsexosomesIL-17netosisneutrophils

Identifiers

PMID35177337
PMCPMC8843421
OpenAlexW4213323232

What OpenQuestion holds

Textmetadata
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.