Evidence map›Paper›PMID 34055794›Full record

ReviewFrontiers in cell and developmental biology2021

Neuroimmune Pathophysiology in Asthma.

Gandhi F Pavón-Romero, Nancy Haydée Serrano-Pérez, Lizbeth García-Sánchez, Fernando Ramírez-Jiménez, Luis M Terán

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
5.6field-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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

  1. A molecular systems architecture of asthma.Frontiers in immunology · 2026
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  16. Neuroplasticity and neuroimmune interactions with type 2 inflammation in asthma.European respiratory review : an official journal of the European Respiratory Society · 2026
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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 1 institution in 1 country.

Gandhi F Pavón-RomeroDepartment of Immunogenetics and Allergy, Instituto Nacional Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.
Nancy Haydée Serrano-PérezDepartment of Immunogenetics and Allergy, Instituto Nacional Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.
Lizbeth García-SánchezDepartment of Immunogenetics and Allergy, Instituto Nacional Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.
Fernando Ramírez-JiménezDepartment of Immunogenetics and Allergy, Instituto Nacional Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.
Luis M TeránDepartment of Immunogenetics and Allergy, Instituto Nacional Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City, Mexico.
Instituto Nacional de Enfermedades Respiratorias · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a chronic inflammation of lower airway disease, characterized by bronchial hyperresponsiveness. Type I hypersensitivity underlies all atopic diseases including allergic asthma. However, the role of neurotransmitters (NT) and neuropeptides (NP) in this disease has been less explored in comparison with inflammatory mechanisms. Indeed, the airway epithelium contains pulmonary neuroendocrine cells filled with neurotransmitters (serotonin and GABA) and neuropeptides (substance P[SP], neurokinin A [NKA], vasoactive intestinal peptide [VIP], Calcitonin-gene related peptide [CGRP], and orphanins-[N/OFQ]), which are released after allergen exposure. Likewise, the autonomic airway fibers produce acetylcholine (ACh) and the neuropeptide Y(NPY). These NT/NP differ in their effects; SP, NKA, and serotonin exert pro-inflammatory effects, whereas VIP, N/OFQ, and GABA show anti-inflammatory activity. However, CGPR and ACh have dual effects. For example, the ACh-M3 axis induces goblet cell metaplasia, extracellular matrix deposition, and bronchoconstriction; the CGRP-RAMP1 axis enhances Th2 and Th9 responses; and the SP-NK1R axis promotes the synthesis of chemokines in eosinophils, mast cells, and neutrophils. In contrast, the ACh-α7nAChR axis in ILC2 diminishes the synthesis of TNF-α, IL-1, and IL-6, attenuating lung inflammation whereas, VIP-VPAC1, N/OFQ-NOP axes cause bronchodilation and anti-inflammatory effects. Some NT/NP as 5-HT and NKA could be used as biomarkers to monitor asthma patients. In fact, the asthma treatment based on inhaled corticosteroids and anticholinergics blocks M3 and TRPV1 receptors. Moreover, the administration of experimental agents such as NK1R/NK2R antagonists and exogenous VIP decrease inflammatory mediators, suggesting that regulating the effects of NT/NP represents a potential novel approach for the treatment of asthma.

Indexed as

allergyasthmaimmunologyneuropeptidesneurotransmitters

Identifiers

PMID34055794
PMCPMC8155297
OpenAlexW3161584948

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.