Evidence map›Paper›PMID 39266756›Full record

ArticleSurgical endoscopy2024

Noninvasive biomarkers for the detection of GERD-induced pulmonary injury.

Andrés R Latorre-Rodríguez, Sumeet K Mittal, Ranjithkumar Ravichandran, Austin Reynolds, Andrés Isaza-Restrepo, Jahanvi Mittal, Mary F Hahn, Ross M Bremner, Thalachallour Mohanakumar

Abstract read
In one paragraph

Article in Surgical endoscopy, 2024. 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. Article
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

9 authors.

Andrés R Latorre-RodríguezNorton Thoracic Institute, St. Joseph's Hospital and Medical Center, 500 W Thomas Road, Phoenix, AZ, 85013, USA.ORCID 0000-0003-3401-8623
Sumeet K MittalNorton Thoracic Institute, St. Joseph's Hospital and Medical Center, 500 W Thomas Road, Phoenix, AZ, 85013, USA. sumeetkmittal@gmail.com.ORCID 0000-0003-2760-3891
Ranjithkumar RavichandranNorton Thoracic Institute, St. Joseph's Hospital and Medical Center, 500 W Thomas Road, Phoenix, AZ, 85013, USA.ORCID 0000-0003-2188-7029
Austin ReynoldsCreighton University School of Medicine, Phoenix Health Sciences Campus, Phoenix, AZ, USA.
Andrés Isaza-RestrepoGrupo de Investigación Clínica, Escuela de Medicina y Ciencias de La Salud, Universidad del Rosario, Bogotá, D.C, Colombia.ORCID 0000-0002-1569-969X
Jahanvi MittalNorton Thoracic Institute, St. Joseph's Hospital and Medical Center, 500 W Thomas Road, Phoenix, AZ, 85013, USA.
Mary F HahnDepartment of Pathology, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
Ross M BremnerNorton Thoracic Institute, St. Joseph's Hospital and Medical Center, 500 W Thomas Road, Phoenix, AZ, 85013, USA.ORCID 0000-0003-2216-9109
Thalachallour MohanakumarNorton Thoracic Institute, St. Joseph's Hospital and Medical Center, 500 W Thomas Road, Phoenix, AZ, 85013, USA.ORCID 0000-0001-9873-4018

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe role of gastroesophageal reflux in progressive lung damage is increasingly recognized. We have proposed, based on our work with lung transplant recipients, a novel immune mechanism of pulmonary injury after aspiration of gastric contents, during which higher levels of normally sequestered lung self-antigens (SAgs) collagen V (Col-V) and K-alpha-1 tubulin (Kα1T) in circulating small extracellular vesicles (EVs) induce the production of self-antibodies (SAbs) anti-Col-V and anti-Kα1T. Thus, we aimed to determine whether levels of SAbs or SAgs increased in an animal model of aspiration-induced lung damage in a nontransplant setting.

methodsWe created a murine model of repetitive lung aspiration using C57BL/6J mice. Mice were aspirated weekly with 1 mL/kg of hydrochloric acid (n = 9), human gastric contents (n = 9), or combined (1:1) fluid (n = 9) once, three, or six times (n = 3 in each subgroup; control group, n = 9). Blood samples were periodically obtained, and all animals were sacrificed at day 90 for pathological assessment. SAbs were measured using an enzyme-linked immunosorbent assay; SAgs and NF-κB contained in small EVs were assessed by western blot.

resultsAspirated mice weighed significantly less than controls throughout the study and had histological evidence of pulmonary injury at day 90. Overall, aspirated mice developed higher concentrations of anti-Col-V at day 28 (53.9 ± 28.7 vs. 29.9 ± 4.5 ng/mL, p < 0.01), day 35 (42.6 ± 19.8 vs. 28.6 ± 7.2 ng/mL, p = 0.038), and day 90 (59.7 ± 27.7 vs. 34.1 ± 3.2 ng/mL, p = 0.014) than the control group. Circulating small EVs isolated from aspirated mice on day 90 contained higher levels of Col-V (0.7 ± 0.56 vs. 0.18 ± 0.6 m.o.d., p = 0.009) and NF-κB (0.42 ± 0.27 vs. 0.27 ± 0.09 m.o.d., p = 0.095) than those from controls.

conclusionsThis experimental study supports the theory that gastroesophageal reflux leads to the development of lung damage and an increase of humoral markers that may serve as noninvasive biomarkers to detect asymptomatic lung injury among patients with gastroesophageal reflux disease.

Indexed as

BiomarkersGastroesophageal RefluxMice, Inbred C57BLAnimalsAutoantibodiesAutoantigensCollagen Type VDisease Models, AnimalHumansLung InjuryMaleMiceTubulinAutoantibodiesAutoantigensBiomarkersCollagen Type VTubulinBiomarkersExtracellular vesiclesGastroesophageal refluxLung injuryProof of concept studyRespiratory aspiration

Identifiers

PMID39266756
PMCPMC11615114

What OpenQuestion holds

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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.