Evidence map›Paper›PMID 32497778›Full record

ArticleBrain, behavior, and immunity2020

A pharmacological interactome between COVID-19 patient samples and human sensory neurons reveals potential drivers of neurogenic pulmonary dysfunction.

Pradipta R Ray, Andi Wangzhou, Nizar Ghneim, Muhammad S Yousuf, Candler Paige, Diana Tavares-Ferreira, Juliet M Mwirigi, Stephanie Shiers, Ishwarya Sankaranarayanan, Amelia J McFarland and 5 more

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  12. Neuro-Immune Interactions in Severe COVID-19 Infection.Pathogens (Basel, Switzerland) · 2022
    Review
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  18. Lung Cancer Models Reveal Severe Acute Respiratory Syndrome Coronavirus 2-Induced Epithelial-to-Mesenchymal Transition Contributes to Coronavirus Disease 2019 Pathophysiology.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2021
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Pradipta R RayUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA. Electronic address: prr105020@utdallas.edu.
Andi WangzhouUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Nizar GhneimUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Muhammad S YousufUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Candler PaigeUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Diana Tavares-FerreiraUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Juliet M MwirigiUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Stephanie ShiersUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Ishwarya SankaranarayananUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Amelia J McFarlandUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Sanjay V NeerukondaUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Steve DavidsonUniversity of Cincinnati, College of Medicine, Department of Anesthesiology, USA.
Gregory DussorUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA.
Michael D BurtonUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Neuroimmunology and Behavior Research Group, USA.
Theodore J PriceUniversity of Texas at Dallas, School of Behavioral and Brain Sciences and Center for Advanced Pain Studies, Pain Neurobiology Research Group, USA. Electronic address: theodore.price@utdallas.edu.
The University of Texas at Dallas · USUniversity of Cincinnati Medical Center · US

Funding

Translation Control of Pain PlasticityR01NS065926 · NINDS · UNIVERSITY OF TEXAS DALLAS · PI PRICE, THEODORE J. · 2010 to 2023
$5.7M
Novel mechanisms regulating protein interaction and painR01NS115441 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI DALVA, MATTHEW B, PRICE, THEODORE J. · 2020 to 2023
$2.1M
The Role of Cell-specific TLR-4 Signaling in Developing Chronic PainK22NS096030 · NINDS · UNIVERSITY OF TEXAS DALLAS · PI BURTON, MICHAEL D · 2016 to 2019
$838k
NINDS NIH HHS K22 NS096030NINDS NIH HHS R01 NS065926NINDS NIH HHS R01 NS115441
6 · The paper itself

Abstract

The SARS-CoV-2 virus infects cells of the airway and lungs in humans causing the disease COVID-19. This disease is characterized by cough, shortness of breath, and in severe cases causes pneumonia and acute respiratory distress syndrome (ARDS) which can be fatal. Bronchial alveolar lavage fluid (BALF) and plasma from mild and severe cases of COVID-19 have been profiled using protein measurements and bulk and single cell RNA sequencing. Onset of pneumonia and ARDS can be rapid in COVID-19, suggesting a potential neuronal involvement in pathology and mortality. We hypothesized that SARS-CoV-2 infection drives changes in immune cell-derived factors that then interact with receptors expressed by the sensory neuronal innervation of the lung to further promote important aspects of disease severity, including ARDS. We sought to quantify how immune cells might interact with sensory innervation of the lung in COVID-19 using published data from patients, existing RNA sequencing datasets from human dorsal root ganglion neurons and other sources, and a genome-wide ligand-receptor pair database curated for pharmacological interactions relevant for neuro-immune interactions. Our findings reveal a landscape of ligand-receptor interactions in the lung caused by SARS-CoV-2 viral infection and point to potential interventions to reduce the burden of neurogenic inflammation in COVID-19 pulmonary disease. In particular, our work highlights opportunities for clinical trials with existing or under development rheumatoid arthritis and other (e.g. CCL2, CCR5 or EGFR inhibitors) drugs to treat high risk or severe COVID-19 cases.

Indexed as

Antirheumatic AgentsBetacoronavirusBronchoalveolar Lavage FluidCoronavirus InfectionsCOVID-19COVID-19 Drug TreatmentCytokinesDatabases, FactualGanglia, SpinalHumansLungMolecular Targeted TherapyNociceptorsPandemicsPneumonia, ViralReceptors, CytokineAntirheumatic AgentsCytokinesReceptors, Cytokine

Identifiers

PMID32497778
PMCPMC7263237
OpenAlexW3023767473

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.