Evidence map›Paper›PMID 39102805›Full record

ArticleDigestion2024

Toll-Like Receptor 7-Expressed Macrophages Are Involved in the Pathogenesis of Esophageal Achalasia and Esophagogastric Junction Outflow Obstruction.

Masatoshi Kaizuka, Tetsuya Tatsuta, Shogo Kawaguchi, Tadashi Yoshizawa, Shukuko Yoshida, Tetsuyuki Tateda, Yohei Sawada, Shinji Ota, Shiro Hayamizu, Keisuke Hasui and 9 more

Abstract read
In one paragraph

Article in Digestion, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

19 authors.

Masatoshi KaizukaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan, m.kaizuka@hirosaki-u.ac.jp.
Tetsuya TatsutaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Shogo KawaguchiDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Tadashi YoshizawaDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Shukuko YoshidaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Tetsuyuki TatedaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Yohei SawadaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Shinji OtaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Shiro HayamizuDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Keisuke HasuiDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Hidezumi KikuchiDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Hiroto HiragaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Daisuke ChindaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Takahiro MuroyaDepartment of Gastroenterological Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Kenichi HakamadaDepartment of Gastroenterological Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Hiroshi KijimaDepartment of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Tatsuya MikamiDepartment of Preemptive Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Shinsaku FukudaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Hirotake SakurabaDepartment of Gastroenterology, Hematology, and Clinical Immunology,,Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionEsophageal achalasia is a typical esophageal motility disorder (EMD). Although viral infections have been hypothesized to play a role in the pathogenesis of esophageal achalasia, its etiology remains unclear. This study used esophageal muscle layer specimens collected during per-oral endoscopic myotomy (POEM) procedures to investigate the association between esophageal achalasia and esophagogastric junction outflow obstruction (EGJOO) and pattern recognition receptors.

methodsPatients with esophageal achalasia and EGJOO who underwent POEM were allocated to the EMD group. Biopsies of the inner circular muscle were conducted during the POEM procedure. The control group comprised individuals diagnosed with esophageal squamous cell carcinoma who underwent surgical resection. Expression of pattern recognition receptors, including Toll-like receptor (TLR) 7, was examined by polymerase chain reaction. Immunohistochemical staining was performed to determine TLR7 expression sites in the esophageal muscle layer, and the relationship between TLR7 mRNA expression and clinical score was investigated.

resultsOur analysis revealed a notable upregulation of TLR7 mRNA levels within the muscle layer of esophageal achalasia and EGJOO, in contrast to those of control specimens. In contrast, the correlation between TLR7 and clinical score was not significant. Immunohistochemical staining revealed increased numbers of TLR7-expressing macrophages between the muscle layers.

conclusionsTLR7-expressing macrophages are involved in the innate immune response underlying esophageal achalasia and EGJOO. This result will lead to the elucidation of new pathogenetic mechanisms and the development of novel therapeutic targets.

Indexed as

Esophageal AchalasiaEsophagogastric JunctionMacrophagesToll-Like Receptor 7AdultAgedCase-Control StudiesEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaEsophagusFemaleHumansImmunohistochemistryMaleMiddle AgedMuscle, SmoothRNA, MessengerTLR7 protein, humanToll-Like Receptor 7Esophageal achalasiaEsophagogastric junction outflow obstructionInnate immunityMacrophagesPOEMToll-like receptor 7

Identifiers

PMID39102805
PMCPMC11633874

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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.