Evidence map›Paper›PMID 41013452›Full record

ArticleJournal of neuroinflammation2025

Eosinophil recruitment and activation in the central nervous system of patients with subarachnoid neurocysticercosis.

Emily Miltenberger, Janitzio Guzmán, Rodaba Rahim, Miranda Yu, Michelle Makiya, Perla Adames Castillo, Soo Ching Lee, Theodore E Nash, Amy D Klion, Thomas B Nutman and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

11 authors.

Emily MiltenbergerLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Janitzio GuzmánLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Rodaba RahimLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Miranda YuLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Michelle MakiyaLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Perla Adames CastilloLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Soo Ching LeeLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Theodore E NashLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Amy D KlionLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Thomas B NutmanLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA.
Elise M O'ConnellLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Division of Intramural Research, 10 Center Dr. Bldg 10 Rm 11N206, Bethesda, MD, 20892, USA. oconnellem@mail.nih.gov.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesSubarachnoid neurocysticercosis (SANCC) is the most severe manifestation of neurocysticercosis. Most complications (communicating hydrocephalus, ischemic stroke, aneurysm, and subarachnoid hemorrhage) are due to inflammation localized to the central nervous system (CNS). The role of eosinophils in the inflammation associated with SANCC has not been previously studied.

methodsCryopreserved CSF collected as part of a clinical trial for neurocysticercosis (NCC) were assessed for analytes associated with eosinophil activation and recruitment using multiplex bead assays in both subjects with SANCC (n = 28) and in NCC-negative controls (n = 26). The SANCC patients underwent chart review for extraction of clinical variables as well as grouping by disease severity to identify analytes that may be associated with the development of more severe symptoms of SANCC.

resultsEosinophil granule proteins (EGPs - ECP, EDN, and EPO), markers of eosinophil activation, were elevated in the CSF of SANCC patients compared to controls. Moreover, the eosinophil-associated cytokines/chemokines IL-5, IL-13, IL-18, CCL24/eotaxin-2, and CCL26/eotaxin-3 were also significantly elevated in the CSF of SANCC patients compared to controls. In those for whom there were paired specimens (n = 13) from baseline and following cure, there was a significant reduction in these cytokines/chemokines (except CCL26/eotaxin-3). The percentage of CSF white blood cells that were eosinophils was positively correlated with EDN, EPO, IL-5, IL-13, CCL24, CCL26, CCL8, CCL13, and CCL5/RANTES, as well as the time it took to achieve biomarker cure. When SANCC patients were subdivided between those with severe disease and those with non-severe disease, the levels of eosinophil cationic protein (ECP), the CCR3 ligands (CCL7 and CCL5), CCL4, IL-18, and IL-1RA discriminated clearly between these 2 groups.  DISCUSSION: These data provide evidence for eosinophil recruitment and activation in the subarachnoid space in patients with SANCC, as well as for a potential role of eosinophils in driving inflammation-associated complications.

Indexed as

Central Nervous SystemEosinophilsNeurocysticercosisAdultAgedBiomarkersCytokinesFemaleHumansMaleMiddle AgedSubarachnoid SpaceYoung AdultBiomarkersCytokinesCysticercosisEosinophilic meningitisEosinophilsHelminthNeurocysticercosisParasite

Identifiers

PMID41013452
PMCPMC12465403

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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.