Evidence map›Paper›PMID 33319634›Full record

ReviewTissue barriers2021

The blood-brain barrier dysfunction in sepsis.

Tatiana Barichello, Jaqueline S Generoso, Allan Collodel, Fabricia Petronilho, Felipe Dal-Pizzol

Open access · bronzeAbstract readReview
In one paragraph

Review in Tissue barriers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 3 pooled it
3.3field-weighted citation impact, top 7% 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

55 citing papers in PubMed, 3 syntheses or guidelines pooled it, 85 citations in OpenAlex.

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  10. From Glycocalyx Shedding to Microvascular Collapse in Sepsis: Endothelial Pathophysiology, Organ Dysfunction, and Mechanistic Biomarkers.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
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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

5 authors at 2 institutions in 2 countries.

Tatiana BarichelloLaboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) , Criciúma, Brazil.
Jaqueline S GenerosoLaboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) , Criciúma, Brazil.ORCID 0000-0003-0571-6764
Allan CollodelLaboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) , Criciúma, Brazil.
Fabricia PetronilhoLaboratory of Neurobiology of Inflammatory and Metabolic Processes, Graduate Program in Health Sciences, Health Sciences Unit, University of South Santa Catarina , Tubarão, Brazil.
Felipe Dal-PizzolLaboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC) , Criciúma, Brazil.
Centro Universitário do Espírito Santo · BRUniversidade do Sul de Santa Catarina · BR

Funding

Infection-driven mechanisms associated with Alzheimer's disease pathologyRF1AG072491 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BARICHELLO, TATIANA, MORALES, RODRIGO · 2021 to 2021
$2.0M
Infection-driven mechanisms associated with Alzheimer's disease pathologyR01AG072491 · NIA · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BARICHELLO, TATIANA, MORALES, RODRIGO · 2024 to 2025
$1.2M
NIA NIH HHS R01 AG072491NIA NIH HHS RF1 AG072491
6 · The paper itself

Abstract

Sepsis is a life-threatening organ dysfunction triggered by a dysregulated host immune response attempting to eliminate the infection. After hospital discharge, half of the sepsis survivors recover, one-third of the patients die the following year, and one-sixth have a long-term cognitive impairment, including memory dysfunction, anxiety, depression, and post-traumatic stress disorder. The infection triggers the host immune response, and both can cause vascular endothelial damage, interrupting tight junctions proteins; consequently, the blood-brain barrier (BBB) breaks down, allowing and facilitating the entry of peripheral immune cells into the brain, which triggers or exacerbates the activation of glial cells and neuroinflammation. The focus of this review is to identify biochemical abnormalities induced by sepsis, which is associated with BBB dysfunction; provide evidence of biomarkers involved in the tight junction disruption and BBB damage, and draw attention to the role of the BBB as a bridge between systemic infection and brain inflammation.

Indexed as

Blood-Brain BarrierHumansSepsisBBBneuroinflammationsepsistight junction protein

Identifiers

PMID33319634
PMCPMC7849782
OpenAlexW3110911296

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.