Evidence map›Paper›PMID 32279287›Full record

ReviewSeminars in thrombosis and hemostasis2020

A Champion of Host Defense: A Generic Large-Scale Cause for Platelet Dysfunction and Depletion in Infection.

Martin J Page, Etheresia Pretorius

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in thrombosis and hemostasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 73 citations in OpenAlex.

  1. Observational
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  15. Biofilm-dispersed pneumococci induce elevated leukocyte and platelet activation.Frontiers in cellular and infection microbiology · 2024
    Article
  16. Article
  17. Pro-Tumorigenic and Thrombotic Activities of Platelets in Lung Cancer.International journal of molecular sciences · 2023
    Review
  18. Article
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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

2 authors at 1 institution in 1 country.

Martin J PageDepartment of Physiological Sciences, Stellenbosch University, Stellenbosch, South Africa.ORCID 0000-0002-2479-9182
Etheresia PretoriusDepartment of Physiological Sciences, Stellenbosch University, Stellenbosch, South Africa.ORCID 0000-0002-9108-2384
Stellenbosch University · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thrombocytopenia is commonly associated with sepsis and infections, which in turn are characterized by a profound immune reaction to the invading pathogen. Platelets are one of the cellular entities that exert considerable immune, antibacterial, and antiviral actions, and are therefore active participants in the host response. Platelets are sensitive to surrounding inflammatory stimuli and contribute to the immune response by multiple mechanisms, including endowing the endothelium with a proinflammatory phenotype, enhancing and amplifying leukocyte recruitment and inflammation, promoting the effector functions of immune cells, and ensuring an optimal adaptive immune response. During infection, pathogens and their products influence the platelet response and can even be toxic. However, platelets are able to sense and engage bacteria and viruses to assist in their removal and destruction. Platelets greatly contribute to host defense by multiple mechanisms, including forming immune complexes and aggregates, shedding their granular content, and internalizing pathogens and subsequently being marked for removal. These processes, and the nature of platelet function in general, cause the platelet to be irreversibly consumed in the execution of its duty. An exaggerated systemic inflammatory response to infection can drive platelet dysfunction, where platelets are inappropriately activated and face immunological destruction. While thrombocytopenia may arise by condition-specific mechanisms that cause an imbalance between platelet production and removal, this review evaluates a generic large-scale mechanism for platelet depletion as a repercussion of its involvement at the nexus of responses to infection.

Indexed as

Blood PlateletsHumansInfections

Identifiers

PMID32279287
PMCPMC7339151
OpenAlexW3015430657

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.